seligman learned helplessness dog experiment video

Learned Helplessness

Charlotte Nickerson

Research Assistant at Harvard University

Undergraduate at Harvard University

Charlotte Nickerson is a student at Harvard University obsessed with the intersection of mental health, productivity, and design.

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Saul McLeod, PhD

Editor-in-Chief for Simply Psychology

BSc (Hons) Psychology, MRes, PhD, University of Manchester

Saul McLeod, PhD., is a qualified psychology teacher with over 18 years of experience in further and higher education. He has been published in peer-reviewed journals, including the Journal of Clinical Psychology.

Olivia Guy-Evans, MSc

Associate Editor for Simply Psychology

BSc (Hons) Psychology, MSc Psychology of Education

Olivia Guy-Evans is a writer and associate editor for Simply Psychology. She has previously worked in healthcare and educational sectors.

Learned helplessness is a psychological state in which an individual, after repeated exposure to uncontrollable negative events, believes they are powerless to change their situation, even when opportunities to do so arise. This leads to passivity, decreased motivation, and a sense of hopelessness, which can persist even when circumstances change and control is possible. Learned helplessness is often associated with depression.

Key Takeaways

• Learned Helplessness is a phenomenon that occurs when a series of negative outcomes or stressors cause someone to believe that the outcomes of life are out of one’s control.
• If a person learns that their behavior makes no difference to their aversive environment, they may stop trying to escape from aversive stimuli even when escape is possible.
• Martin Seligman and Steven F. Maier first identified learned helplessness as a phenomenon in the 1960s. These psychologists conducted experiments on dogs, finding that, when exposed to repeated shocks that they could not control, the animals refrained from taking action when they could prevent the shocks.
• Learned helplessness has notably been linked to and used as an explanation for depression and post-traumatic stress disorder in humans, but not without criticism.
• There are a number of ways to overcome learned helplessness. One mentioned by Seligman himself is learned hopefulness.

What Is Learned Helplessness?

Learned Helplessness is a phenomenon where repeated exposure to uncontrollable stressors results in people failing to use any methods to control their response to those stressors that are at their disposal in the future.

Essentially, those experiencing learned helplessness are said to learn that they lack behavioral control over the events in their environment, which, in turn, undermines their motivation to make changes or attempt to alter situations.

The first people to describe learned helplessness were the American psychologists Steven F. Maier and Martin E. P. Seligman.

Martin Seligman conducted a series of classic experiments in the 1960s (Seligman & Maier, 1967). Some dogs were placed in a chamber where they received electric shocks from which they could not escape (the non-escape condition).

The dogs in the escape group could escape the shocks by pressing a panel with their nose.

In the second phase, the animals were placed in a shuttle box divided by a barrier in the middle so that the dogs could jump in order to escape the shocks. Only the dogs that had learned to escape in the previous phase tried to jump. The other dogs did not.

When the dogs in the “non-escape” condition were given the opportunity to escape the shocks by jumping across a partition, most failed even to try; they seemed just to give up and passively accept any shocks the experimenters chose to administer.

In comparison, dogs who were previously allowed to escape the shocks tended to jump the partition and escape the pain.

3 symptoms of learned helplessness

Martin Seligman, the psychologist who first described learned helplessness, identified three main features that characterize this behavior:

• Lack of motivation: When faced with new challenges or difficult situations, people with learned helplessness often fail to respond or even try. They feel like giving up before they start and have a low tolerance for even the smallest bumps in the road.
• Difficulty learning from success : Even when people with learned helplessness manage to cope with a situation successfully, they have trouble learning from that experience. They don’t see their success as a sign that they can handle similar challenges in the future.
• Emotional numbness : People with learned helplessness may seem less affected by painful or stressful events. They might appear to be emotionally flat or unresponsive.

However, later research found that even though people with learned helplessness might seem emotionally numb on the outside, they are actually experiencing high levels of stress on the inside.

Scientists discovered this by measuring cortisol levels, a stress hormone, in their blood (Ackerman, 2022).

Is learned helplessness a mental health condition? 

Learned helplessness is not a diagnosable mental health condition but a thought disorder characterized by problematic thinking patterns that lead to maladaptive behavior.

Although not a standalone disorder, learned helplessness can feature in or exacerbate other mental health conditions such as anxiety, depression, phobias, and loneliness.

Symptoms of learned helplessness, including low motivation, perceived lack of control, and low self-esteem, overlap with those of depression and anxiety.

In the 1970s, Seligman extended the concept of learned helplessness from nonhuman animal research to clinical depression in humans and proposed a learned helplessness theory to explain how people become vulnerable to depression.

According to this theory, people who are repeatedly exposed to stressful situations beyond their control develop an inability to make decisions or engage effectively in purposeful behavior.

Subsequently, researchers have noticed that this learned helplessness theory is similar to posttraumatic stress disorder (Ackerman, 2022).

The Role of Explanatory Styles in Learned Helplessness

Although the initial learned helplessness theory was considered an important breakthrough in its time, it soon became accepted that the theory needed further development to apply to humans, who are more complex than other animals in terms of their cognitive processes.

Seligman and colleagues later reformulated the original learned helplessness model of depression (Abramson, Seligman, & Teasdale, 1978).

In their reformulation, they emphasized attributions (i.e., a mental explanation for why something occurred) that lead to the perception that one lacks control over negative outcomes and are important in fostering a sense of learned helplessness.

The explanatory style model of learned helplessness seeks to identify patterns in individual reactions to positive and negative events and occurrences in their lives.

The model’s logic is that when individuals find themselves in a situation where something has gone either right or wrong, they will ask why.

The answers that that person tends to give when asking themselves that kind of question will dictate whether that person defaults to an optimistic or pessimistic explanatory style (Healy, 2017).

Unhelpful : When a negative event occurs, if someone believes that the cause of the event is stable or long-lasting, this perspective can lead to chronic feelings of helplessness.

Helpful : When a negative event occurs, if someone believes that the cause is temporary, this perspective can reduce feelings of helplessness.

Unhelpful : If a person believes that the cause of a negative event will impact multiple areas of their life, they may be more susceptible to experiencing widespread helplessness.

Helpful : If a person believes that the cause of a negative event is specific to the issue at hand and will not affect other areas of their life, they will be less likely to experience helplessness.

Unhelpfu l: If someone attributes the cause of a negative event to their own actions or characteristics (an internal cause) rather than external factors, it can have negative consequences for their self-esteem.

In their writing on explanatory styles, Martin Seligman and Christopher Peterson (1967) stressed that one’s explanatory style will tend to follow a pattern. That means that someone will tend to respond to positive and negative events in consistent, habitual ways.

This can be very advantageous to someone’s well-being if they happen to default to an optimistic explanatory style, but very problematic for those who tend toward pessimism.

In fact, learned helplessness and a pessimistic explanatory style are each linked with the development of depression in individuals (Healy, 2017).

Optimistic vs. Pessimistic Explanatory Styles

The markers of an optimistic explanatory style stand in direct contrast to those signaling their pessimistic counterpart.

• For example, while the pessimistic style can view negative circumstances as something that will inevitably persist and positive occurrences as temporary, the optimistic style tends to view negative circumstances as temporary and expects positive occurrences to persist.
• Additionally, while the negative explanatory style tends toward self-blame for outcomes that go awry and credit external factors when things go right, the positive style leads to individuals crediting themselves when things go right and identifying external factors as key when things go wrong (Healy, 2017).

Nonetheless, moderation is required in considering the extent to which an optimistic explanatory style is the most beneficial for overcoming learned helplessness.

For example, always defaulting to blaming others or circumstances when things go wrong and always attributing successes as exclusively one’s doing can, while meeting the criteria for the optimistic explanatory style, constitute a problem in itself (Healy, 2017).

Overcoming Learned Helplessness

Ultimately, Learned helplessness provides an explanation for human behaviors that may otherwise seem odd or counterproductive, and understanding learned helplessness provides pathways to removing or reducing its negative impacts (Ackerman, 2022).

Focus on what you can control

Focusing on what you can control is a powerful way to combat learned helplessness. When you feel like everything is out of your control, it’s easy to give up and feel helpless.

But by shifting your focus to the things you can influence, you can start to regain a sense of power over your life.

For example, you might not be able to control whether or not you get a promotion at work, but you can control how much effort you put into your job.

You can’t control the weather, but you can control how you prepare for and respond to it.

Here are some things you can control:

• Your attitude : Choose to approach challenges with a positive, can-do mindset.
• Your effort : Decide how much time and energy you put into your goals.
• Your response : You can’t always control what happens to you, but you can control how you react to it.
• Your self-care : Prioritize taking care of your physical and mental health.
• Your relationships : Nurture the relationships that bring positivity into your life.

By focusing on these areas, you remind yourself that you have the power to influence your life, even in small ways.

This can help combat the feeling of helplessness and give you the confidence to tackle bigger challenges over time.

Learned optimism

Learned optimism, a concept introduced by Martin Seligman, is the antithesis of learned helplessness.

While learned helplessness involves internalizing a sense of hopelessness about one’s circumstances, learned optimism encourages individuals to challenge their negative thought processes and adopt a more positive outlook.

By doing so, people can change their behaviors and ultimately, their outcomes.

The process of developing learned optimism involves recognizing and questioning the automatic negative thoughts that contribute to feelings of helplessness.

When faced with a challenge or setback, individuals with learned optimism actively reframe their thoughts, looking for alternative explanations and solutions rather than defaulting to self-blame or despair.

For example, instead of thinking, “I failed because I’m not good enough,” a person practicing learned optimism might think, “This was a tough situation, but I can learn from it and do better next time.”

By consistently challenging negative self-talk and focusing on the aspects of a situation they can control, individuals can gradually shift their mindset from one of helplessness to one of resilience and empowerment.

Cultivating learned optimism takes time and practice, but it can have a profound impact on an individual’s well-being, motivation, and ability to overcome challenges.

By adopting a more optimistic outlook, people can break free from the cycle of learned helplessness and take active steps toward creating positive change in their lives.

Learn from failures

Carol Dweck, a psychologist, has found another powerful way to reduce learned helplessness, and it involves experiencing failure. In her research, Dweck divided people into two groups:

• The first group was given tasks that were designed for them to fail. After failing, they were told to take responsibility for their failure and to believe that it happened because they didn’t put in enough effort.
• The second group was given tasks that were easy enough for them to succeed every time. They never experienced failure during the study.

The results of Dweck’s (1975) study were interesting. The group that only experienced success showed no changes in how they reacted to failure later on. They still had extreme, negative reactions when they failed at something.

However, the group that experienced failure and was taught to take responsibility for it showed big improvements. They didn’t react as badly when they failed at something later on.

In simple terms, this study suggests that experiencing failure and learning to see it as a result of not trying hard enough, rather than a lack of ability, can help people overcome learned helplessness.

It teaches them that failure isn’t permanent and that they have the power to change the outcome next time by putting in more effort.

Learned hopefulness

Learned hopefulness is a concept that emphasizes the importance of empowering experiences in helping individuals overcome learned helplessness.

It suggests that by providing opportunities for people to learn new skills and develop a sense of control over their lives, they can become more resilient in the face of everyday challenges and barriers.

Unlike learned optimism, which focuses on changing thought patterns, learned hopefulness emphasizes the role of actual experiences in shaping one’s outlook and ability to cope with difficulties.

When individuals are exposed to situations that allow them to successfully navigate challenges, they develop a sense of mastery and control. This, in turn, helps them approach future obstacles with greater confidence and determination.

By fostering learned hopefulness through supportive environments and skill-building opportunities, individuals can break free from the cycle of learned helplessness and develop a more empowered, proactive approach to life.

This resilience can serve as a buffer against the negative effects of stress and adversity.

Overparenting and learned helplessness

Overparenting, often associated with “helicopter parents,” can inadvertently contribute to developing learned helplessness in adulthood.

When parents consistently intervene and solve their children’s problems, children may become overly dependent on their parents’ support.

This dependency can lead to a fear of failure and a belief that they are incapable of succeeding without their parent’s help.

While it can be difficult for parents to watch their children struggle, experiencing routine failures and challenges is essential to growing up.

These experiences teach children valuable skills such as problem-solving, coping with disappointment, and building resilience.

By facing and overcoming obstacles on their own, children develop a sense of self-efficacy and learn that they can navigate difficult situations.

While well-intentioned, overparenting can deprive children of these crucial learning opportunities, potentially leading to learned helplessness and a lack of confidence in their own abilities as adults.

Learned helplessness in education

Learned helplessness is a common subject of interest in the field of education. In particular, educators are interested in how early academic failure or low academic self-esteem can impact later success and how the relationship can be influenced to enhance chances of success (Firmin, Hwang, Copella, & Clark, 2004).

Learned helplessness in students creates a cycle where those who feel they are unable to succeed are unlikely to put effort into schoolwork. This, in turn, decreases their chances of success, leading to even less motivation and effort.

This cycle can culminate in a student having almost no motivation to learn a subject and no competence.

It can even lead to a more generalized sense of helplessness in which the student has no belief in their ability and no motivation to learn any subject at school (Firmin, Hwang, Copella, & Clark, 2004).

Educators have developed a few strategies that can help prevent students from learning to be habitually helpless, such as:

Providing praise and encouragement based on the student’s abilities to help them believe they are good at these subjects.

Providing praise and encouragement based on a student’s efforts.

Working on individual goal-setting with students to help them learn that goals can be achieved and that outcomes can be in their control (Firmin, Hwang, Copella, & Clark, 2004).

Learned helplessness in relationships

Learned helplessness is also of interest to researchers focused on domestic violence, as it’s often observed in relationships involving abuse.

The phenomenon of learned helplessness has helped researchers answer questions such as why those who are abused do not tell others, try to get help or leave the relationships (Ackerman, 2022).

Often, in abusive relationships, abusers subject their victims to repeated abuse to acclimatize the victims to the abuse and teach them that they do not have control over the situation.

The abusers, as a result, maintain complete control, and the victims learn that they are helpless about their circumstances (Ackerman, 2022). Often, these perceptions are very difficult to get rid of, often requiring intensive therapy and support (Ackerman, 2022).

Studies of learned helplessness in humans

Although experiments that are as extreme as Seligman’s have not been performed on humans — and would not pass ethically — experiments performed on humans have produced similar outcomes.

In one study of learned helplessness in humans, participants were split into three groups. One group was subjected to a loud and unpleasant noise but was able to end the noise by pressing a button four times, while the second group was subjected to the same noise, but the button was not functional.

Everyone was then given a box with a lever which, when manipulated, would turn off the sound. As in the animal experiments, those who had no control over the noise in the first part tended not even to try to turn the noise off, while the other participants did (Seligman, 1967; Ackerman, 2022).

Learned hopefulness at volunteer organizations

One example of an environment where individuals can learn hopefulness is voluntary organizations. Someone working at an after-school center, tutoring young children in mathematics and Seligman’s may be encouraged to see how their presence leads to students directly developing a better grasp of school material.

This may have run-off effects in other areas of the participant’s life. Zimmerman (1990) conducted a study of how empowered individuals felt after volunteering consistently in such environments, as measured by cognitive, personality, and motivational measures of perceived control.

He found that those who volunteered felt more in control of their own lives and were more likely to attribute their successes to their own actions (Zimmerman, 1990).

Criticisms of Learned Helplessness

Seligman’s original (1967) learned helplessness theory, as well as the reformulations of others, have received a number of criticisms.

Psychologists believe that there is more to depression than learned helplessness. While the symptoms of learned helplessness may mirror those of depression, there is an array of complex neurological and psychological factors underlying the condition.

Indeed, depression may not necessarily arise from a repeat failure.

For example, students may become depressed after repeatedly blaming themselves for chronic school stress and poor exam results.

Additionally, those in learned helplessness experiments have often described their task as skill tasks despite acting as if they were chance tasks.

That is to say, people participating in these learned helplessness experiments, while seemingly behaving as if they have no control over the outcome, have been known to say verbally that they still believe that their effort can influence its outcomes (Ackerman, 2022).

Abramson, L. Y., Seligman, M. E., & Teasdale, J. D. (1978). Learned helplessness in humans: critique and reformulation .  Journal of abnormal psychology ,  87 (1), 49.

Ackerman, C. (2022). Learned helplessness: Seligman’s Theory of Depression .

Dweck, C. S. (1975). The role of expectations and attributions in the alleviation of learned helplessness. Journal of personality and social psychology, 31 (4), 674.

Firmin, M. W., Hwang, C. E., Copella, M., & Clark, S. (2004). Learned helplessness: The effect of failure on test-taking. Education, 124 (4), 688.

Healy, C. (2017). Learned Helplessness & Explanatory Style .

Maier, S. F., & Seligman, M. E. (2016). Learned helplessness at fifty: Insights from neuroscience . Psychological Review, 123 (4), 349.

Seligman, M. E., & Maier, S. F. (1967). Failure to escape traumatic shock. Journal of experimental psychology, 74 (1), 1.

Seligman, M. E. (1972). Learned helplessness .  Annual review of medicine ,  23 (1), 407-412.

Thompson, J. A. (2010). Learned helplessness: You’re not trapped .

Zimmerman, M. A. (1990). Toward a theory of learned hopefulness: A structural model analysis of participation and empowerment. Journal of research in personality, 24 (1), 71-86.

• Psychology , Psychology Experiments

Learned Helplessness Experiment: Doggone Attitudes

Your coach has introduced a new training method: at practice, you’ll jump hurdles while wearing weights on your legs. The idea is that after training for a while, you’ll be able to jump much higher and run much faster once the weights are off. You’re not so sure it will actually work though. Running is hard but not impossible. Jumping, however, earns you a tangled mess of limbs every time. You try different techniques, but it makes no difference. You get a few bruises on your elbow and even a skinned knee. After a week, your coach asks you to take off the weights and try jumping the hurdles without them. You get in position at the starting line and sprint to the hurdle. All you can think of is the pain of the last few falls and before you know it, you’re on the ground. Your coach is confused. “You jumped right into the hurdle - you didn’t even try to clear it.”

Somewhere in the back of your mind, you know objectively you’re capable of doing the jump. But the weight training has conditioned you to think that you can’t. Since you always fall and injure yourself with the weights on, you start to think it will always happen even when the weights are off. You perceive this suffering and failure as permanent, so you make no effort to stop it from happening.

Learned Helplessness

Learned helplessness is a phenomenon in which after experiencing pain or discomfort in an inescapable situation, an animal or human will cease trying to avoid the suffering. They have learned that they are helpless - they believe they have no control over their situation, even if there is an opportunity to escape. This kind of conditioning was famously studied in Seligman’s Learned Helplessness Experiment.

The Experiment

The notable part of the experiment was conducted in 1967 at the University of Pennsylvania by Martin Seligman and his colleagues. However, it only came about because two years prior, the researchers had been experimenting with classical conditioning, which is the process by which an animal or human comes to associate one stimulus with another. Seligman experimented with dogs: first a bell would be rung and then the dog would receive a shock. After a number of pairings, the dogs were classically conditioned - once they heard the bell, they’d react as if they’d already been shocked. 

Seligman later crafted a box with a low fence dividing its middle. One side was electrified while the other was not. The dog could easily see and jump over the fence. Seligman predicted that if a dog was placed on the electrified section, it would simply jump to safety. However, when he used the dogs from the earlier experiment as test subjects, nearly all of them did not move. They laid down on the electrified section they were placed on.

Seligman brought in a new set of animals and found that dogs who had not experienced the first classical conditioning would always jump over the fence. He concluded that the original set of dogs had learned to be helpless - they had no control in the first half of the experiment, so they assumed they would never have control. They believed there was nothing they could do to avoid the shocks, even when there was a clear option they could take to do so. Seligman called this condition “learned helplessness.”

Applying It

Learned helplessness has been observed in humans and animals. If bad things constantly happen outside of your control, you’re liable to start thinking you can never prevent them from happening. This is the case with victims of abuse, from physical to verbal to emotional. Even when escape seems possible, many won’t leave an abusive relationship or home because they think it won’t do them any good - they’ll get caught and end up right back where they started. It’s also been discussed that learned helplessness likely plays a strong role in depression and other mental illnesses. If you think you’re not in control, you believe your actions will make no difference. Just like one of Seligman’s classically conditioned dogs, you’ll lie down and give up.

But not every one of those dogs did lie down. Some still jumped the fence despite being test subjects in the first half of the experiment. Seligman later theorized that whether someone experiences learned helplessness has to do with the strength and type of their explanatory style. A pessimistic explanatory style involves personal blame for bad outcomes and beliefs that such suffering is permanent and pervasive. Meanwhile, an optimistic one involves external blame for negative events and beliefs that such suffering is temporary and local. For example, someone with an optimistic explanatory style might say, “I didn’t make the team because I didn’t practice hard enough.” The negative event is attributed to a lack of effort, something that can easily be remedied. Meanwhile, someone with a pessimistic explanatory in the same situation might say, “I didn’t make the team because I’m not good enough.” The suffering is internalized - the person believes they are inherently lackluster and can never remedy the situation. 

These outlooks play an important role. They serve almost as self-fulfilling prophecies. If you’re optimistic and perceive your situation as malleable, you will take every opportunity to change it for the better and will likely do so because you don’t give up. If you’re pessimistic and perceive your situation as fixed, you won’t bother to try to affect it and thus stay stuck in bad situations. Your outlook affects your end goals. 

Finally, it should be noted that Seligman and his colleagues did eventually get the conditioned dogs to jump over the fence. They tried many methods, but the only one that worked was picking up the dogs and moving their legs, replicating the actions the dogs themselves would need to perform to escape the electrified side. They needed to do this at least twice, i.e. create a pattern of realistic escape, before the dog would jump on its own. When someone is depressed or suffering, saying “things will get better” does no one any good. Rather, it’s better to physically show that friend that their suffering isn’t global and that they can still find happiness multiple times until they can accept that as truth on their own.

Think Further

• Why do you think Seligman’s findings were so ground-breaking?
• Who would you expect to have more success, better health, and lower rates of depression — those with optimistic or pessimistic explanatory styles? Explain your answer.
• Taking from Seligman’s experiments, what are some ways you can help someone realize they have control over a bad situation?

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What Causes Learned Helplessness?

Verywell / Nusha Ashjaee 

Learned Helplessness in Children

• Mental Health Conditions
• How to Overcome It

Learned helplessness occurs when a person who has experienced repeated challenges comes to believe they have no control over their situation. They then give up trying to make changes and accept their fate.

In animals , learned helplessness occurs when an animal is repeatedly subjected to an aversive stimulus that it cannot escape. Eventually, the animal will stop trying to avoid the stimulus and behave as if it is utterly helpless to change the situation. Even when opportunities to escape are presented, this learned helplessness will prevent any action.

While the concept is strongly tied to animal psychology and behavior, it can also apply to many situations involving human beings. When people feel that they have no control over their situation, they may begin to behave in a helpless manner. This inaction can lead people to overlook opportunities for relief or change.

For example, poor performance at work or at school, even after putting in a lot of effort, can lead to feelings of learned helpless. People may be left feeling that no matter what they do or how hard they work, nothing will make a difference.

This article discusses the signs of learned helplessness and the research that led to the term being coined. It also explores what causes this type of behavior and strategies that can help people overcome it.

Symptoms of Learned Helplessness

Everyone can struggle at times, especially when coping with adversity and setbacks. Learned helplessness is characterized by more lasting symptoms such as:

• Avoiding decisions
• Bad attitude
• Giving up quickly
• Inability to tolerate frustration
• Lack of effort
• Low motivation
• Passive behavior
• Poor self-esteem
• Procrastination
• Refusing to try

Learned helplessness is not a mental health condition, but it can sometimes be a sign of a mental disorder such as depression or anxiety.

The Discovery of Learned Helplessness

The concept of learned helplessness was discovered accidentally by psychologists  Martin Seligman  and Steven F. Maier. They had initially observed helpless behavior in dogs that were classically conditioned to expect an electrical shock after hearing a tone.

Later, the dogs were placed in a shuttlebox that contained two chambers separated by a low barrier. The floor was electrified on one side, and not on the other. The dogs previously subjected to the  classical conditioning  made no attempts to escape, even though avoiding the shock simply involved jumping over a small barrier.

To investigate this phenomenon, the researchers then devised another experiment.

• In group one , the dogs were strapped into harnesses for a period of time and then released.
• In group two , the dogs were placed in the same harnesses but were subjected to electrical shocks that could be avoided by pressing a panel with their noses.
• In group three , the dogs received the same shocks as those in group two, except that those in this group were not able to control the shock. For those dogs in the third group, the shocks seemed to be completely random and outside of their control.

The dogs were then placed in a shuttlebox. Dogs from the first and second group quickly learned that jumping the barrier eliminated the shock. However, those from the third group made no attempts to get away from the shocks.

In Seligman and Maier's experiments, the dog's who were unable to escape the shocks developed learned helplessness. Due to their previous experience, they had developed a cognitive expectation that nothing they did would prevent or eliminate the shocks.

Causes of Learned Helplessness

Learned helplessness is frequently the result of experiencing stress or trauma . People may feel that they have little to no control over the situation. Because of the lack of control, people may feel helpless and unmotivated to take action.

Common causes that can lead to learned helplessness include:

• Childhood neglect
• Difficult 
• Domestic violence
• Natural disasters

Overparenting can also contribute to the development of learned helplessness in children. When children are not allowed to try things independently, they may develop a poor sense of personal agency. Instead of trying, they believe that they are unable to do things and do not put forth any effort.

The three elements of learned helplessness are contingency, cognition, and behavior. Contingency refers to the belief that there is a relationship between events and behaviors, cognition refers to how people think about these relationships, and behavior refers to the actions they take as a result of observing the relationship between actions and events.

The Role of Explanatory Styles

So what explains why some people develop learned helplessness and others do not? Why is it specific to some situations but more global in others?

Attribution or explanatory styles may also play a role in determining how people are impacted by learned helplessness. This view suggests that an individual's characteristic style of explaining events helps determine whether or not they will develop learned helplessness.

A pessimistic explanatory style is associated with a greater likelihood of experiencing learned helplessness. People with this explanatory style tend to view negative events as being inescapable and unavoidable and tend to take personal responsibility for such negative events.

Impact of Learned Helplessness

The impact of learned helplessness has been demonstrated in different animal species, but its effects can also be seen in people.

Consider one often-used example: A child who performs poorly on math tests and assignments will quickly begin to feel that nothing they do will have any effect on their math performance. When later faced with any type of math-related task, they might feel hopeless and unable to do the work.

Learned helplessness has also been associated with several different psychological disorders. Depression, anxiety,  phobias , shyness, and  loneliness  can all be exacerbated by learned helplessness.

For example, feeling shy in social situations can cause people to feel that there is nothing they can do to overcome their symptoms. Because symptoms feel out of control, people may stop trying to engage themselves in social situations, thus making their shyness even more pronounced.

Researchers have found, however, that learned helplessness does not always generalize across all settings and situations.

A student who experiences learned helplessness with regards to math class will not necessarily experience that same helplessness when faced with performing calculations in the real world. In other cases, people may experience learned helplessness that generalizes across a wide variety of situations.

Learned helplessness often originates in childhood, and unreliable or unresponsive caregivers can contribute to these feelings. This learned helplessness can begin very early in life. Children raised in institutionalized settings, for example, often exhibit symptoms of helplessness even during infancy.

When children need help but no one comes to their aid, they may be left feeling that nothing they do will change their situation. Repeated experiences that bolster these feelings of helplessness and hopelessness can result in growing into adulthood ultimately feeling that there is nothing one can do to change his or her problems.

Some common symptoms of learned helplessness in children include:

• Failure to ask for help
• Frustration
• Low self-esteem
• Poor motivation

Learned helplessness can also result in anxiety, depression, or both. When kids feel that they've had no control over the past events of their lives, they gain the expectation that future events will be just as uncontrollable. Because they believe that nothing they do will ever change the outcome of an event, kids are often left thinking that they should not even bother trying.

Academic struggles can also potentially lead to feelings of learned helplessness. A child who makes an effort to do well but still does poorly may end up feeling that they have no control over their grades or performance.

Since nothing they do seems to make any difference, they will stop trying and their grades may suffer even more. Such problems can also affect other areas of the child's life. Their poor performance in school can make them feel that nothing they do is right or useful, so they may lose the motivation to try in other areas of their life as well.

Learned Helplessness and Mental Health

Learned helplessness may also contribute to feelings of anxiety and may influence the onset, severity, and persistence of conditions such as generalized anxiety disorder (GAD).

When you experience chronic anxiety, you may eventually give up on finding relief because your anxious feelings seem unavoidable and untreatable. Because of this, people who are experiencing mental health issues such as anxiety or depression may refuse medications or therapy that may help relieve their symptoms.

As people age learned helplessness can become something of a vicious cycle. When encountering problems such as anxiety or depression, people may feel that nothing can be done to ease these feelings.

People then fail to seek out options that may help which then contributes to greater feelings of helplessness and anxiety.

Overcoming Learned Helplessness

So what can people do to overcome learned helplessness? Learned helplessness can often be successfully decreased, particularly if intervention occurs during the early stages. Long-term learned helplessness can also be reduced, although it may require longer-term effort. Strategies that can help include:

Psychotherapy

Therapy can be effective in reducing symptoms of learned helplessness. Cognitive-behavioral therapy  is a form of psychotherapy that can be beneficial in overcoming the thinking and behavioral patterns that contribute to learned helplessness.

The goal of CBT is to help patients identify negative thought patterns that contribute to feelings of learned helplessness and then replace these thoughts with more optimistic and rational thoughts. This process often involves carefully analyzing what you are thinking, actively challenging these ideas, and disputing negative thought patterns.

Self-Care Strategies

One animal study suggested that exercise may help reduce symptoms of learned helplessness. Other self-care strategies, such as getting enough sleep, managing stress levels, and eating a healthy diet, can also help people foster a greater sense of control over their life.

Social Support

Getting social support and encouragement from others may also be helpful. When you feel helpless in the face of a challenge, supportive people can help you feel more motivated and encouraged to keep trying. With time and continued practice, you can eventually acquire successful experiences that help you feel more in control.

A Word From Verywell

Learned helplessness can have a profound impact on mental health and well-being. People who experience learned helplessness are also likely to experience symptoms of depression , elevated stress levels, and less  motivation  to take care of their physical health.

Not everyone responds to experiences the same way. Some people are more likely to experience learned helplessness in the face of uncontrollable events, often due to biological and psychological factors. Children raised by helpless parents, for example, are also more likely to experience learned helplessness.

If you feel that learned helplessness might be having a negative impact on your life and health, consider talking to your doctor about steps you can take to address this type of thinking.

Further evaluation can lead to an accurate diagnosis and treatment that can help you replace your negative thought patterns with more positive ones. Such treatment may allow you to replace feelings of learned helplessness with a sense of learned optimism instead.

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By Kendra Cherry, MSEd Kendra Cherry, MS, is a psychosocial rehabilitation specialist, psychology educator, and author of the "Everything Psychology Book."

Learned Helplessness: Seligman’s Theory of Depression

Even outside the field of psychology, it’s pretty widely understood.

It provides an explanation for some human behaviors that might seem odd or counterproductive, and understanding learned helplessness provides pathways to removing or reducing its negative impacts.

Learned helplessness was discovered through some well-known laboratory experiments that you might have learned about in a Psychology 101 class. Those experiments were conducted using methods that likely would horrify any reasonable member of an institutional review board today.

Although it has been about 50 years since learned helplessness became a well-understood psychological theory, it still looms large in the field. If you’re interested in learning more about this important concept, you’ve come to the right place. This article will cover what learned helplessness is, what impact it can have on a person’s life, how to neutralize or reverse that impact, and how to measure one’s degree of learned helplessness.

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This Article Contains:

What is learned helplessness a psychological definition.

• Martin Seligman’s Experiments That Led to the Theory

Examples of Learned Helplessness in Humans

Learned helplessness and depression.

• It’s Most Likely to be Associated With . . .
• It’s Most Likely to Promote . . .

Learned Helplessness in Education

Learned helplessness in relationships and domestic violence, learned helplessness: the book, a possible cure—potential treatments for children and adults.

• Seligman’s Learned Optimism Model

Relevant Tests, Scales, and Questionnaires

Relevant youtube videos, most interesting research, a take-home message.

Learned helplessness is a phenomenon observed in both humans and other animals when they have been conditioned to expect pain, suffering, or discomfort without a way to escape it (Cherry, 2017). Eventually, after enough conditioning, the animal will stop trying to avoid the pain at all—even if there is an opportunity to truly escape it.

When humans or other animals start to understand (or believe) that they have no control over what happens to them, they begin to think, feel, and act as if they are helpless.

This phenomenon is called learned helplessness because it is not an innate trait. No one is born believing that they have no control over what happens to them and that it is fruitless even to try gaining control. It is a learned behavior, conditioned through experiences in which the subject either truly has no control over his circumstances or simply perceives that he has no control.

Martin Seligman’s Experiments That Led to the Theory

These experiments will be described in detail below. Please note that some readers may find the descriptions upsetting—such experiments were more commonplace in the ’60s and ’70s, but they would likely meet lots of resistance from activists and the general public today.

Seligman and Maier were working with dogs at the time and testing their responses to electrical shocks. Some of the dogs received electrical shocks that they could not predict or control.

For this experiment, the dogs were placed in a box with two chambers divided by a low barrier. One chamber had an electrified floor and the other was not (Cherry, 2017).

When the researchers placed dogs in the box and turned on the electrified floor, they noticed a strange thing: Some dogs didn’t even attempt to jump over the low barrier to the other side. Further, the dogs who didn’t attempt to jump the barrier were generally the dogs who had previously been given shocks with no way to escape them, and the dogs who jumped the barrier tended to be those who had not received such treatment.

To further investigate this phenomenon, Seligman and Maier gathered a new batch of dogs and divided them into three groups:

• Dogs in Group One were strapped into harnesses for a period of time and were not administered any shocks;
• Dogs in Group Two were strapped into the same harnesses but were administered electrical shocks that they could avoid by pressing a panel with their noses;
• Dogs in Group Three were placed in the same harnesses and also administered electrical shocks, but were given no way to avoid them.

Once these three groups had completed this first experimental manipulation, all dogs were placed (one at a time) in the box with two chambers. Dogs from Group One and Group Two were quick to figure out that they only needed to jump over the barrier to avoid the shocks, but most of the dogs from Group Three didn’t even attempt to avoid them.

Based on their previous experience, these dogs concluded that there was nothing they could do to avoid being shocked (Seligman & Groves, 1970).

Once these results had been confirmed with dogs, Seligman and Maier conducted similar experiments on rats. Just as they did with dogs, the researchers split the rats into three groups for training: One group received escapable shocks, one received inescapable shocks, and one received no shocks at all.

The rats in the group that received escapable shocks were able to avoid shocks by pressing a lever in the box, while those in the group receiving inescapable shocks could press the lever, but would still receive shocks (Seligman & Beagley, 1975).

Later, the rats were placed in a box and received electrical shocks. A lever was present within the box that, when pressed, would allow the rats to escape the shocks.

Again, rats who were initially placed in the inescapable shock group generally did not even attempt to escape, while most of those rats in the other two groups succeeded in escaping.

The rats who did not attempt to escape were showing behavior that is classic to learned helplessness: even when presented with a potential option to avoid pain, they do not attempt to take it.

This phenomenon can also be seen in elephants. When an elephant trainer starts working with a baby elephant, he or she will use a rope to tie one of the elephant’s legs to a post. The elephant will struggle for hours, even days, trying to escape the rope, but eventually, it will quiet down and accept its range of motion (Wu, 2009).

When the elephant grows up, it will be more than strong enough to break the rope, but it won’t even try—it’s been taught that any kind of struggle is useless.

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Such extreme experiments have not been performed on humans (nor should they), the experiments that have been conducted on humans have produced similar outcomes. Although the human response to such situations may be more complex and dependent on several different factors, it still resembles the responses of dogs, rats, and other animals.

One study of learned helplessness in humans was conducted in 1974. In that study, the human participants were split into three groups: One group was subjected to a loud and unpleasant noise but was able to terminate the noise by pressing a button four times; the second group was subjected to the same noise, but the button was not functional; and the third group was subjected to no noise at all.

Later, all human participants were subjected to a loud noise and given a box with a lever which, when manipulated, would turn off the sound. Just like in the animal experiments, those who had no control over the noise in the first part of the experiment generally did not even try to turn the noise off, while the rest of the subjects generally figured out how to turn the noise off very quickly.

Seligman and colleagues proposed that subjecting participants to situations in which they have no control results in three deficits: motivational, cognitive, and emotional (Abramson, Seligman, & Teasdale, 1978). The cognitive deficit refers to the subject’s idea that his circumstances are uncontrollable. The motivational deficit refers to the subject’s lack of response to potential methods of escaping a negative situation.

Finally, the emotional deficit refers to the depressed state arises when the subject is in a negative situation that he feels is not under his control.

Based on his research, Seligman found an important connection: the link between learned helplessness and depression.

Universal helplessness is a sense of helplessness in which the subject believes nothing can be done about the situation she is in. She believes no one can alleviate the pain or discomfort.

On the other hand, personal helplessness is a much more localized sense of helplessness. The subject may believe others could find a solution or avoid the pain or discomfort, but he believes that he, personally, is incapable of finding a solution (Abramson, Seligman, & Teasdale, 1978).

Both types of helplessness can lead to a state of depression, but the quality of that depression may differ. Those who feel universally helpless will tend to find external reasons for both their problems and their inability to solve them, while those who feel personally helpless will tend to find internal reasons.

In addition, those who feel personally helpless are more likely to suffer from low self-esteem since they believe others could probably solve the problems they feel incapable of solving.

Although the cognitive and motivational deficits are the same for people suffering from both personal and universal helplessness, people experiencing personal helplessness tend to have a greater and more impactful emotional deficit.

In addition to this differentiation between types of helplessness, learned helplessness can on two other factors: generality (global vs. specific) and stability (chronic vs. transient).

When a person suffers from global helplessness , they experience negative impacts in several areas of life, not just the most relevant area. They are also more likely to experience severe depression than those who experience  specific helplessness .

Further, those suffering from chronic helplessness (those who have felt helpless over a long period of time) are more likely to feel the effects of depressive symptoms than those who experience transient helplessness (a short-lived and nonrecurrent sense of helplessness).

This model of learned helplessness has important implications for depression. It posits that when highly desired outcomes are believed to be improbable and/or highly aversive outcomes are believed probable, and the individual has no expectation that anything she does will change the outcome, depression results.

However, the depression will vary based on the type of helplessness. The range of depressive symptoms will depend on the generality and stability of the helplessness, and any impact on self-esteem is dependent on how the individual explains or attributes their experience (internally vs. externally).

This proposed framework identifies the cause of at least one type of depression—that which stems from helplessness—and provides the path to a cure for it. The researchers outlined four strategies for treating helplessness-related depression (Abramson, Seligman, & Teasdale, 1978):

• Change the likelihood of the outcome. Alter the environment by increasing the likelihood of desired events and decreasing the likelihood of negative events;
• Reduce the desire for preferred outcomes. This can be done by either reducing the negativity of events that are outside the individual’s control or by reducing the desirability of events that are extremely unlikely to happen;
• Change the individual’s expectation from uncontrollability to controllability when the desired outcomes are attainable. In other words, help the depressed person realize when outcomes they desire are actually within their control;
• Change unrealistic explanations for failure toward those that are external (not due to some inherent flaw in the depressed person himself), transient (not chronic), and specific (due to one specific problem rather than a larger pattern of problems). Likewise, change unrealistic explanations for success to those that are internal (due to some inherent strength in the depressed person), stable (chronic), and global (due to an overall competence rather than a specific area of competence).

These strategies will be covered in more detail later.

It’s Likely to Be Associated With . . .

Learned helplessness is, unsurprisingly, associated with many negative symptoms, traits, and tendencies, including:

• Age: The older one’s age, the more likely they are to experience change or loss of roles and physical decline. Residing in an institution is also linked to learned helplessness (Foy & Mitchell, 1990);
• Stress, especially poverty-related stress (Brown, Seyler, Knorr, Garnett, & Laurenceau, 2016);
• Anxiety and worry, specifically about tests for students (Raufelder, Regner, & Wood, 2018);
• Greater negative response to anticipated pain (Strigo, Simmons, Matthews, Craig, & Paulus, 2008).

It’s Most Likely to Promote…

Not only is learned helplessness often associated with other negative conditions, but it also seems to contribute to or cause many negative outcomes, including:

• Negative health symptoms as well as  negative emotions about one’s disease (Nowicka-Sauer, Hajduk, Kujawska-Danecka, Banaszkiewicz, Czuszyńska, Smoleńska, & Siebert, 2017);
• Maladaptive perfectionism (Filippello, Larcan, Sorrenti, Buzzai, Orecchio, & Costa, 2017);
• Turnover intentions (Tayfur, Karapinar, & Camgoz, 2013);
• Burnout , or emotional exhaustion and cynicism (Tayfur et al., 2013);
• Aggravated depression, anxiety, phobias, shyness, and loneliness in those already suffering (Cherry, 2017).

The topic of learned helplessness comes up quite regularly in the education field.

There’s quite a bit of interest in how early academic failure or low academic self-esteem  can impact later success, and how the relationship can be influenced to enhance chances of success.

Learned helplessness in students creates a vicious cycle. Those who feel that they are unable to succeed are unlikely to put much effort into their schoolwork, which decreases their chances of success, leading to even less motivation and effort (Catapano, n.d.).

This vicious cycle may culminate in a student having virtually no motivation to learn a subject and no competence in that subject. Even worse, it could lead to a more generalized sense of helplessness in which the student has no belief in her ability and no motivation to learn any subject at school.

The reasons students give to explain their failure or success is critical in school. If a student believes he failed because the teacher hates him or he’s simply stupid, he is blaming factors that are not within his control and is likely to develop a greater sense of helplessness.

If a student believes she failed because she didn’t study hard enough, she is blaming factors that are within her control, which is much less likely to lead to an overall sense of helplessness related to school.

Luckily, there are a few strategies that can help prevent students from learning to be habitually helpless, including:

• Teachers providing praise and encouragement based on the student’s abilities (e.g., “You’re good at math” or “You have a knack for this subject, I can tell”) to help them believe they are good at these tasks or subjects;
• Teachers providing praise and encouragement based on the student’s efforts (e.g., “Your hours of hard work paid off on this test!”) to help them believe their effort will make a difference;
• Working on smart, individual goal-setting with students to help them learn that goals can be achieved and that outcomes are often within their realm of influence (Catapano, n.d.).

In addition, Edutopia’s Andrew Miller (2015) suggests a few very important strategies for teachers and parents:

• Curate and create learning resources (which include people, books, websites, and community organizations, among other resources) to help students become comfortable with not knowing the answer and with looking for the answer in the right places;
• Use questions for learning rather than about learning (e.g., use questions that encourage the student to think about his own learning and thought patterns instead of just thinking about what he knows);
• Stop giving students the answers. Instead, help them learn it at their own pace and through their own methods—they’ll be more likely to remember it this way!
• Allow them to fail. Failing and trying again is vital for children—as long as you are there to support them when they fail.

In addition to these strategies, later on in this piece we’ll discuss some insights into treating or “curing” learned helplessness that can be applied to students.

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In addition to education, learned helplessness comes up often for people focused on domestic violence. It’s often observed in relationships and in victims of domestic violence.

In fact, this phenomenon has helped us find an answer to some of the questions people have for victims who stay with their abusers, such as:

• Why didn’t they tell someone?
• Why didn’t they try to get help?
• Why didn’t they just leave?

It’s hard to explain the impact of abuse on the victim’s behavior. After all, observers might think it makes no sense that victims choose to stay with someone who is hurting them.

However, in cases of domestic violence and abuse, abusers often administer a series of “electrical shocks” (i.e., the form of abuse they subject their victims to) to acclimatize the victims to the abuse and teach them that they do not have control over the situation. The abusers maintain complete control, and the victims learn that they are helpless about their circumstances.

In such cases, it is easy to see how abuse can lead to learned helplessness, which can subsequently lead to a lack of motivation or effort to escape on the victim’s part. Just as the dogs in Seligman and Maier’s experiments learned that no matter what they did, they would be shocked, the victims of domestic violence and abuse learn that no matter what they do, they will always remain powerless and under the abusers’ control.

These perceptions are incredibly hard to shake, often requiring intensive therapy and support in order to shake them.

Based on learned helplessness, a specific theory was developed for victims of domestic violence called the theory of cyclic abuse, a cycle that is sometimes known as battered women syndrome. In this theory, a relationship in which domestic violence has occurred is likely to continually involve violence that’s doled out in a predictable and repetitious pattern.

This pattern generally follows this structure:

• Stage One: a period of tension-building in which the abuser starts to get angry, communication breaks down, and the victim feels the need to concede and submit to the abuser;
• Stage Two: the acting-out period, in which the abuse occurs;
• Stage Three: the honeymoon period, in which the abuser may apologize, show remorse, and/or try to make up for the abuse. The abuser might also promise never to abuse the victim again or, alternatively, blame the victim for provoking the abuse;
• Stage Four: the calm period, in which the abuse stops, the abuser acts like it never happened, and the victim may start to believe the abuse has ended and the abuser will change (Rakovec-Felser, 2014).

Viewed from this perspective, it’s not surprising that many victims of domestic violence develop learned helplessness. When the abuse is inflicted upon them in a continuing cycle, no matter what they do, they are likely to feel completely helpless and unable to avoid the abuse.

The theory of cyclic abuse posits that not only will abuse victims feel helpless, they will also:

• Re-experience the battering as if it were recurring even when it is not;
• Attempt to avoid the psychological impact of battering by avoiding activities, people, and emotions;
• Experience hyperarousal or hypervigilance;
• Have disrupted interpersonal relationships;
• Experience body image distortion or other somatic concerns;
• Develop sexuality and intimacy issues (Rakovec-Felser, 2014).

Clearly, learned helplessness is a serious and urgent concern for victims of domestic violence and other abuse. Luckily, there are some ways to treat learned helplessness (see the section on treatments).

It chronicles the studies that prompted the theory of learned helplessness and provides a cogent and comprehensive summary of the research up to the book’s publication (in 1995) on the phenomenon. It outlines the connection between learned helplessness and depression as well as investigating other facets, like the cognitive and biological aspects.

If you are looking for a deeper dive into this topic, this book will provide you with an informative overview of learned helplessness. You can find it for purchase here .

While learned helplessness can be hard to overcome, there exist promising treatments to address it in humans (and in other animals, for that matter).

One potential treatment based on  neuroscience  research is the relationship between the ventromedial prefrontal cortex (a part of the brain that plays a role in the inhibition of emotional responses) and the dorsal raphe nucleus (a part of the brainstem associated with serotonin and depression) and learned helplessness (Maier & Seligman, 2016).

This potential treatment may focus on stimulating the ventromedial prefrontal cortex and inhibiting the dorsal raphe nucleus through medication, electrical stimulation, or trans-magnetic stimulation, or psychologically through therapy.

Trans-magnetic stimulation (TMS) in particular has been shown in recent studies to be quite effective in the treatment of depression (Mayo Clinic, 2017). Given the link between learned helplessness and depression, it makes sense to think that a treatment for one may be an effective treatment for the other.

Speaking of effective treatments for depression, therapy is also a good choice for people struggling with learned helplessness. Those who feel helpless can benefit from working with a licensed mental health professional to explore the origins of their helplessness, replace old and harmful beliefs with newer and healthier beliefs, and develop a healing sense of compassion for themselves (Thompson, 2010).

Insightful research from psychologist Carol Dweck (the researcher who went on to propose the theory of growth vs. fixed mindset) showed that there is another extremely effective way to alleviate learned helplessness: through failure.

In Dweck’s 1975 study on the subject, participants (who all experienced extreme reactions to failure) were split into two groups: one received intensive training in which they failed tasks and were instructed to take responsibility for their failure and attribute it to a lack of effort, while the other group received intensive training in which they only experienced success.

The results showed that those in the success-only treatment group showed no improvement in their extreme reactions to failure, while the group that failed showed a marked improvement.

This experiment was one of several studies throughout the 1970s, 1980s, and 1990s that laid the foundation for a new theory of human behavior related to failure, learned helplessness, and resilience.

Seligman’s Learned Optimism Model

Although Seligman’s name was synonymous with learned helplessness for many years, he knew he had a lot more to offer the world. His work on the subject led him to wonder what other mindsets and perspectives can be learned and whether people could develop positive traits instead of developing feelings of helplessness.

Seligman’s research led him to create the model of learned optimism . He found that, through resilience training, people can learn to develop a more optimistic perspective. This ability has been observed in children, teachers, members of the military, and more (Seligman, 2011).

It might not be as easy to learn optimism as it is to learn helplessness, but it can be done. If you’re interested in learning more about optimism and how it can be learned, check out Seligman’s book Learned Optimism: How to Change Your Mind and Your Life at this link . In addition to getting a brief overview of the research on this subject, you will also read about several simple techniques you can apply to develop a more positive and self-compassionate explanatory style .

Although many people have included measures of learned helplessness in their studies, they are often informal measures. However, there are two measures that have been used fairly often and/or recently.

The Learned Helplessness Scale (LHS) was developed by Quinless and Nelson (1988) to capture and calculate a score for learned helplessness. The scale is composed of 20 items rated on a scale from 1 (strongly agree) to 4 (strongly disagree). The minimum score on this measure is 20 and the maximum score is 80, with higher scores indicating a greater degree of learned helplessness.

The Learned Helplessness Questionnaire (LHQ) was created in Sorrenti and colleagues’ 2014 study on learned helplessness and mastery orientation. The LHQ consists of 13 items rated on a scale from 1 (not true) to 5 (absolutely true), for a total possible score between 13 and 65. An example item from this scale is the statement, “When you encounter an obstacle in schoolwork you get discouraged and stop trying. You are easily frustrated.”

If you’d like to use any of these scales for research purposes, please refer to the original scale development article for more information.

There are a number of great talks on learned helplessness and/or learned optimism for you to peruse.

For example, Martin Seligman’s TED Talk titled The New Era of Positive Psychology has become a classic, and for good reason. You can watch it here:

There’s also a great video on YouTube from psychologist Lance Luria on the differences between learned helplessness and learned optimism. You’ll learn about the amazing ability of the human brain to train itself, as well as the benefits of meditation , mindfulness , and other ways to link the health of the mind and body.

For an engaging and entertaining look at Seligman’s book Learned Optimism, check out the video below. It’s an animated review of the book that hits all the salient points in under five minutes.

It’s been about five decades since the very first studies on learned helplessness, but there is still interesting new research coming out on the subject.

For instance, in 2017 researchers discovered that, although learned helplessness has been observed in honey bees, they don’t display the “freezing” behavior that other species do (Dinges et al., 2017).

In 2016, researchers in Brazil found some evidence that even zebrafish experience learned helplessness (do Nascimento et al., 2016).

Not even the simple tree shrew is safe from the effects of learned helplessness—research from 2016 confirmed the presence of such behavior in tree shrews who received uncontrollable shocks to the foot (Meng et al., 2016).

In terms of more broadly applicable research on learned helplessness, many recent experiments are probing the link between learned helplessness and the brain.

An oft-cited study from researchers Kim and colleagues (2016) showed that brain activity in mice displaying non-helpless behavior was generally much higher than that of the helpless mice. However, this pattern was reversed in the part of the brain known as the locus coeruleus, which is involved in physiological responses to stress and panic.

This finding is interesting, as it suggests that individuals experiencing learned helplessness are directing their energy toward responding to their own distress, while more resilient individuals keep their energy more normally distributed.

Research on the cellular basis of learned helplessness-related depression has shown that increased activity of the lateral habenula neurons (an area of the brain involved in communications between the forebrain and midbrain structures) in rats is associated with increased learned helplessness behavior (Li et al., 2011).

The implications of connecting learned helplessness to activity in specific parts of the brain are potentially huge; these findings could contribute to new and more effective methods of treating and preventing depression.

This is the kind of exciting research that is happening right now—research that could have huge impacts on treating disorders and healing those who have suffered. Keep an eye out for the fascinating findings that continue to result from this line of research.

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In this piece, we defined learned helplessness, went over the experiments that laid the foundation for the theory, discussed the known associations and outcomes of learned helplessness, and dove into potential treatments for this harmful condition, including strategies to build learned optimism instead of helplessness.

If this piece sparked your curiosity about the subject that goes beyond this piece, we encourage you to check out the sources referenced here in greater detail.

What are your thoughts on learned helplessness? Do you recognize some symptoms in yourself or in your clients? How do you usually address it? Let us know your thoughts in the comments.

We hope you enjoyed reading this article. Don’t forget to download our three Resilience Exercises for free .

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So helpful!

Hi, isn’t it true that SF Maier and M. Seligman say that actually helplessness is not learned, but default? “The mechanism of learned helplessness is now very well-charted biologically and the original theory got it backwards. Passivity in response to shock is not learned. It is the default, unlearned response to prolonged aversive events and it is mediated by the serotonergic activity of the dorsal raphe nucleus, which in turn inhibits escape. This passivity can be overcome by learning control, with the activity of the medial prefrontal cortex, which subserves the detection of control leading to the automatic inhibition of the dorsal raphe nucleus. So animals learn that they can control aversive events, but the passive failure to learn to escape is an unlearned reaction to prolonged aversive stimulation. In addition, alterations of the ventromedial prefrontal cortex-dorsal raphe pathway can come to subserve the expectation of control. ” Maier, S. F., & Seligman, M. E. P. (2016). Learned helplessness at fifty: Insights from neuroscience

Where can I find the details of these strategies?

Hi Valeria,

Thanks for your question! Toward the end of the article, the author outlined potential treatments for children and adults under the heading ‘A Possible Cure’.

Alternatively, you can also read the original article here for more information on treating helplessness-related depression.

I hope this helps!

Kind regards, -Caroline | Community Manager

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learned helplessness , in psychology , a mental state in which an organism forced to bear aversive stimuli , or stimuli that are painful or otherwise unpleasant, becomes unable or unwilling to avoid subsequent encounters with those stimuli, even if they are “escapable,” presumably because it has learned that it cannot control the situation.

The theory of learned helplessness was conceptualized and developed by American psychologist Martin E.P. Seligman at the University of Pennsylvania in the late 1960s and ’70s. While conducting experimental research on classical conditioning , Seligman inadvertently discovered that dogs that had received unavoidable electric shocks failed to take action in subsequent situations—even those in which escape or avoidance was in fact possible—whereas dogs that had not received the unavoidable shocks immediately took action in subsequent situations. The experiment was replicated with human subjects (using loud noise as opposed to electric shocks), yielding similar results. Seligman coined the term learned helplessness to describe the expectation that outcomes are uncontrollable.

Learned helplessness has since become a basic principle of behavioral theory, demonstrating that prior learning can result in a drastic change in behaviour and seeking to explain why individuals may accept and remain passive in negative situations despite their clear ability to change them. In his book Helplessness (1975), Seligman argued that, as a result of these negative expectations, other consequences may accompany the inability or unwillingness to act, including low self-esteem , chronic failure, sadness, and physical illness. The theory of learned helplessness also has been applied to many conditions and behaviours, including clinical depression , aging, domestic violence , poverty , discrimination , parenting, academic achievement, drug abuse , and alcoholism . Critics, however, have argued that a variety of different conclusions can be drawn from Seligman’s experiments and therefore broad generalizations, most frequently found in the areas of clinical depression and academic achievement, are unwarranted. For example, the application of the theory to clinical depression is viewed as an oversimplification of the illness that fails to account for the complex cognitive processes involved in its etiology , severity, and manifestation .

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Learned Helplessness at Fifty: Insights from Neuroscience

Steven f. maier.

University of Colorado

Martin E. P. Seligman

University of Pennsylvania

Learned helplessness, the failure to escape shock induced by uncontrollable aversive events, was discovered half a century ago. Seligman and Maier (1967) theorized that animals learned that outcomes were independent of their responses—that nothing they did mattered – and that this learning undermined trying to escape. The mechanism of learned helplessness is now very well-charted biologically and the original theory got it backwards. Passivity in response to shock is not learned. It is the default, unlearned response to prolonged aversive events and it is mediated by the serotonergic activity of the dorsal raphe nucleus, which in turn inhibits escape. This passivity can be overcome by learning control, with the activity of the medial prefrontal cortex, which subserves the detection of control leading to the automatic inhibition of the dorsal raphe nucleus. So animals learn that they can control aversive events, but the passive failure to learn to escape is an unlearned reaction to prolonged aversive stimulation. In addition, alterations of the ventromedial prefrontal cortex-dorsal raphe pathway can come to subserve the expectation of control. We speculate that default passivity and the compensating detection and expectation of control may have substantial implications for how to treat depression.

In the early 1960s, Richard Solomon and his students at the University of Pennsylvania wanted to know how prior Pavlovian fear conditioning would influence later instrumental learning. To find out they restrained dogs in a hammock and the dogs got 64 mild-moderate electric shocks to their back paws, each shock heralded by a tone. Twenty-four hours later the dogs were placed in a shuttlebox and were supposed to learn to escape shock by jumping a short barrier between the two chambers. The two-factor theory of avoidance learning predicted that turning on the fear-inducing tone in the shuttlebox would generate fear and accelerate jumping. But to the experimenters' annoyance, they could not test this because the dogs often failed to escape altogether in the shuttlebox and passively waited the shock out ( Leaf, 1964 ; Overmier & Leaf, 1965 ).

We arrived at Penn as first year graduate students in 1964. We thought that a profound failure to escape was the phenomenon and we began to try to understand it. After fifty years of research we believe we finally do understand it and this paper presents the evolution and destination of our theory.

From the beginning we thought the phenomenon looked like helplessness, as first suggested by Overmier and Seligman in 1967 . But what, we puzzled, could helplessness consist of? How did it come about? How could we test for it?

Defining Helplessness

The intuitive notion of helplessness entails, we reasoned, the belief that nothing one does matters. This decomposes into objective and subjective helplessness. More formally, an animal is objectively helpless with respect to an important outcome (O) such as shock offset if the probability of (O), given a response (R) is not different from the probability of (O) given the absence of that response (notR). When this is true of all responses, objective helplessness exists.

But being subjectively helpless is another matter. We theorized that helplessness was cognitive and that it was learned. The animal must “detect” the lack of contingency as defined above and so must have “expected” that in the future shock would be independent of its responses. This was a radical suggestion for the 1960s. The learning theories of that era held that organisms could only learn associations or pairings, for example a response paired with shock strengthened this association (acquisition) or a response paired with no shock weakened this association (extinction). The rationale for the narrow associationistic view stemmed from behaviorists' shunning cognitions in animals and it seemed that the integration of two conditional probabilities—the probability of shock given a response integrated with the probability of shock in the absence of that response and then generalized across all responses—must be highly cognitive. Importantly we called the theory “learned” helplessness, rather than “conditioned” helplessness, because integrating these two conditional probabilities did not seem compatible with the associationistic premise that both Pavlovian conditioning and instrumental learning held dear. Emblematic of the tension between learning theory and cognitive theory was an encounter at the Princeton conference in which we first laid the theory out to the major learning theorists ( Maier, Seligman & Solomon, 1969 ): Richard Herrnstein, a prominent Harvard Skinnerian, retorted, “You are proposing that animals learn that responding is ineffective. Animals learn responses ; they don't learn that anything.”

Operationalizing Learned Helplessness

The triadic design to be described operationalizes this definition of objective and subjective learned helplessness. In order to know that it is the non-contingency between responding and shock and not the shock itself that produces later passivity, the non-contingency has to be isolated from the shock. So three groups are needed. One group gets escapable shock (ESC) where shock offset is contingent on the animal's response. So in the original stressor controllability experiment ( Seligman & Maier, 1967 ), this group of dogs learned in the hammock to press a panel with their noses to turn off each shock. The second group is yoked to the ESC group. In this initial experiment, on each trial the yoked group subjects received the average duration of shock that the ESC group produced on each trial. However, in most subsequent experiments described below the yoking was done on each trial for each pair of subjects (ESC and yoked), so that the 2 groups receive exactly the same duration, intensity, and pattern of shocks, but for the yoked subjects their responses have no effect on the shock. In this inescapable shock group (INESC) shock offset and all of the animal's response are non-contingently related. A third group (0) gets no shock.

The next day the animals are tested in a very different environment – shuttlebox escape – and the well-replicated result was that two-thirds of the animals from the INESC group failed to learn to escape, whereas 90% of the animals in both the ESC and 0 groups easily learned to escape. Importantly the ESC and the 0 group learned to escape equally well . We concluded from this result that the animals in the INESC group had learned in the hammock that shock offset was independent of their responses and when shock occurred the next day in the shuttlebox they expected that its offset would once again be independent of responding. This expectation undermined their trying (“response initiation”) to escape. The fact that the escapable shock group did not do better than the zero group and that the main effect was that the inescapable group did worse than both other groups strongly influenced our belief that helplessness had been learned. It should be noted that at almost exactly the same time Weiss (1968) used a similar paradigm to study the effects of coping on ulcer formation.

In one variant Maier (1970) found that the passivity was not a superstitiously acquired response. The contiguity-minded learning theorists countered the cognitive account by claiming that in the hammock, shock offset occasionally was paired with not moving in the INESC group and this “superstitiously” reinforced the association of not moving with shock offset. Hence in the shuttlebox the animals engaged in not moving and eventually shock went off – further strengthening the superstitious no-movement—shock-off association. So Maier ran a special escapable shock group in the hammock: For this group shock went off when the animal held still, explicitly reinforcing not moving—one step better than superstition. The cognitive theory predicted that these animals would not sit still in the shuttlebox since they had learned that they could control shock; whereas the associationistic theory predicted that they would show the competing response of “helplessness.” This was a crucial test of contiguity versus cognition and Maier found that this escapable shock group easily learned to escape in the shuttlebox by jumping the barrier. Hence we discarded contiguity accounts of helplessness.

This work led us to define a dimension that we called control over outcomes , with control being present whenever the probability of (O), given a response (R) is different from the probability of (O) given the absence of that response (notR). Clearly, the escapable subjects have control over an aspect of the aversive event (when each shock terminates), and the inescapable subjects do not. This was exactly why we used the triadic design and included the escapable subjects as a control group because it isolated the element of uncontrollability—if failure to escape in the shuttlebox was caused by learning uncontrollability, then this failure should not occur if uncontrollability is removed but shock stays constant. That is, we assumed that uncontrollability is the active ingredient in producing passivity, and that escapable subjects were later normal because they lacked this critical learning ingredient. The escapable group was thus really included as a control group.

We must mention that running dog experiments was a harrowing experience for both of us. We are both dog lovers and as soon as we could we stopped experimenting with dogs and used rats, mice, and people in helplessness experiments, with exactly the same pattern of results. The next section provides a brief summary of this early work.

Research with animals quickly switched from dogs to rodents, but using the same triadic design that compares exactly equal ESC, yoked INESC, and no shock. Behavioral work focused on two issues. The first issue was whether the later effects of IS are limited to the induction of passivity in tasks such as the shuttlebox. To summarize briefly, a wide range of other behavioral changes followed INESC including reduced aggression, reduced social dominance, reduced food and water intake, exaggerated attention to external cues, reduced preference for sweet tastes, potentiated fear conditioning, slowed fear extinction, neophobia, anxious behavior on measures such as juvenile social exploration, potentiated opioid reward, exaggerated stereotypy to stimulants, and others. Importantly, none of these occurred if the shocks were escapable (see Maier & Watkins, 2005 , for a review). Clearly, some of these outcomes can be related to passivity but others cannot. Many of these other behaviors seem indicative of anxiety, by which we mean fear out of proportion to an existing threat—potentiated fear conditioning, reduced fear extinction, neophobia, reduced juvenile social exploration, avoidance of open arms on an elevated maze, etc. In this paper for simplicity, we will refer to this suite of changes as “passivity/anxiety,” but we emphasize that we are interested in all of the changes separately—but not for the purpose of the present theorizing.

The second issue concerned testing the learned helplessness hypothesis against a variety of alternative ideas that were developed to explain why the experience of INESC leads to later failure to learn to escape in a different environment and whether control/lack of control is the critical underlying dimension (summarized in Maier & Seligman, 1976 ). Most of these investigations were focused on why INESC produces consequences such as failure to learn to escape, not why ESC did not do so. Indeed, the ESC group was typically omitted as this was not deemed of interest. In one important exception, Volpicelli, Ulm, Altenor, and Seligman (1983) using a triadic design found that the ESC group was much superior to the zero group and the INESC group. During later inescapable shock, the ESC group which had first learned to bar press to escape shock continued to run in a shuttlebox during long duration inescapable shock. This learned “mastery” effect foreshadows the main findings of the neuroscientific work below, in which first learning about escapable shock inhibits the default response of passivity. The work of R. L. Jackson and T. Minor was an exception. They argued that INESC produces later behavioral changes because it produces intense fear during the INESC session. With ESC however, the organism has a “safety signal” in that proprioceptive and other feedback from the escape response is followed by a shock-free interval of time. Indeed, these stimuli are as far away from the next shock as possible, and such stimuli do become conditioned inhibitors of fear ( Maier, Rapaport, & Wheatley, 1976 ). This was argued to greatly reduce the total fear experienced during the session, and therefore no later behavioral “symptoms” ( Jackson & Minor, 1988 ; Minor, Trauner, Lee, & Dess, 1990 ; Weiss, 1971 ). Note that by this view there is no learning about uncontrollability or controllability, just Pavlovian processes and fear. As support, the addition of external stimuli such as a light or a tone occurring immediately after each INESC prevented the occurrence of later failure to learn to escape ( Minor et al., 1990 ; Weiss, 1971 ).

The early 1970s witnessed the first research directed at understanding the neural basis of these phenomena. Of course, these investigations could use only the neuroscience tools then available, and for the most part they involved either the systemic or intracerebroventicular administration of various receptor agonists and antagonists, and a role for a number of receptors and their endogenous ligands (e.g., acetylcholine, norepinephrine, dopamine, serotonin, and adenosine) was suggested ( Anisman, Remington, & Sklar, 1979 ; Glazer, Weiss, Pohorecky, & Miller, 1975 ; Petty & Sherman, 1979 ). Given the nature of these studies no particular circuitry or structures could be implicated. However, the work of J. Weiss was an exception. He and his colleagues showed that INESC depletes norepinephrine (NE) in the region of the locus coeruleus (LC), a brainstem cell cluster that provides NE to most of the forebrain. Locus coeruleus NE neurons express alpha-2 receptors on their soma and dendrites, and these are inhibitory autoreceptors. Thus, NE within the locus coeruleus restrains the activity of locus coeruleus neurons, and so depletion of NE within this structure actually increases the activity of NE neurons, and Weiss had shown this to be important in the development of learned helplessness, a phenomenon he called behavioral depression (see Weiss & Simson, 1988 , for review). However, it was never entirely clear how or why increased activity of these neurons would produce the passivity or anxiety. In sum, by the mid-1980s, there were nascent neurochemical views, but their detailed mechanism(s) of operation were necessarily murky given the tools that were then available, and their relationship to behavioral explanations unclear.

From this point on, we each went off to do other things. Seligman began to study humans exclusively. The human work went in three directions.

First, guided by the original theory, the learned helplessness procedures were replicated in apparently analogous human settings (e.g., Hiroto & Seligman, 1975 ). In the triadic design, for example, one group of college students received loud noise that could be escaped by button pressing, a second group was yoked, and a third group received nothing. Then they went to a human shuttlebox in which moving the hand from one side to the other turned off the noise. As with dogs and rats, most of the people from the yoked group failed to escape in the shuttlebox, whereas people from the escapable group and the zero group escaped well in the shuttlebox. Importantly the same pattern in the shuttlebox emerged when preceded by solvable and unsolvable anagrams (and no anagrams) instead of loud noise. In these studies, subjective unsystematic reports occasionally revealed that people from the inescapable group said that “nothing worked so why try?”

The second direction that Seligman took explored and manipulated the explanations people made for the causes of their failure to escape in the inescapable group ( Abramson, Seligman, & Teasdale, 1978 ; Alloy, Peterson, Abramson, & Seligman, 1984 ). In the “attributional reformulation” of learned helplessness, Abramson et al. (1978) claimed that inescapability itself was not sufficient to produce anything more than momentary helplessness. Rather, the explanations that subjects made of the causes of their helplessness predicted the time course and the extent of helplessness. Subjects who attributed their helplessness to permanent causes (e.g., these problems will always be unsolvable) would show long-term helplessness in that situation. In contrast subjects who attributed their helplessness to temporary causes (e.g., only verbal puzzles are unsolvable) would not show helplessness later in that situation. Subjects who attributed their helplessness to pervasive factors (e.g., most problems are unsolvable) would show passivity across situations, whereas subjects who attributed helplessness to local factors (e.g., this problem is unsolvable) would only show helplessness in the original situation. These predictions were tested and largely borne out ( Alloy et al., 1984 ).

The third endeavor that Seligman pursued was the possibility that learned helplessness was a laboratory model of clinical depression ( Seligman, 1974 ; Simson & Weiss, 1988 ). In the Diagnostic and Statistical Manual of the American Psychiatric Association Third Edition ( DSM-III ; American Psychiatric Association, 1980 ), and Fourth Edition ( DSM-IV ; American Psychiatric Association, 1994 ), major depressive disorder was diagnosed by the presence of at least 5 of the following 9 symptoms:

• Loss of interest
• Weight loss
• Sleep problems
• Psychomotor problems
• Worthlessness
• Indecisiveness or poor concentration
• Thoughts of suicide

Learned helplessness in the laboratory – combining the animal and human experimental results – produced eight of the nine symptoms, with the only exception being suicide and suicidal thoughts—an unlikely symptom to be produced in the laboratory by mild aversive events. Not only did inescapable shock and noise produce the symptoms of depression, but the converse occurred as well: Depressed people, who had not received inescapable events, behaved in the laboratory as if they had—showing passivity in the shuttlebox and giving up on cognitive problems ( Klein, Fencil-Morse, & Seligman, 1976 ; Klein & Seligman, 1976 ; Miller & Seligman, 1976 ). Overall learned helplessness by mapping into the symptoms of depression seemed like a plausible laboratory model.

After 2000, Seligman went in two further new directions: First he began to work on “Positive Psychology,” the study of the causes and consequences of positive events ( Seligman & Csikszentmihalyi, 2000 ), among them having control as opposed to being helpless. Second, he began to work on “prospection,” the study of mental simulations and evaluations of possible futures, in contrast to the study of memory (the past) and perception (the present) ( Seligman, Railton, Baumeister, & Sripada, 2013 ). As it turns out both these new directions are relevant to the unraveling of learned helplessness and we will return to positive psychology and prospection at the end of this paper.

Maier essentially switched fields, retrained, and went into neuroscience. As a neophyte neuroscientist he felt that issues of learned helplessness were too complicated to approach and he studied a variety of other phenomena. He eventually returned to learned helplessness and its neural basis. It is this body of work that illuminates uncontrollability much better than the original theory.

Here are the mechanisms that were assumed by the original theory:

First: DETECT: Animals DETECT the dimension of controllability and uncontrollability. (This was also called the dimension of contingency and non-contingency).

Second: EXPECT. Animals that DETECT uncontrollability EXPECT shock or other events to be once again uncontrollable in new situations and this undermines trying to escape in new situations.

This paper examines these two premises in the light of the neural evidence accumulated over the last two decades. We preview the new theory and its conclusions now to help the psychologically-minded reader go through the systematic neural evidence that follows.

First: PASSIVITY/ANXIETY. Aversive shock, among its other neural actions, activates serotonergic (5-HT) neurons in the dorsal raphe nucleus (DRN). The dorsal raphe nucleus sends 5-HT projecting neurons to numerous regions including the periaqueductal gray, striatum, and extended amygdala. 5-HT released in the periaqueductal gray and striatum acts at 5-HT receptors to inhibit active escape behavior , while 5-HT released in the amygdala acts at receptors to potentiate fear/anxiety . The intense activation of the dorsal raphe nucleus by shock sensitizes these neurons and this sensitization lasts for a few days and results in poor escape (passivity) and heightened anxiety. The excitation of the dorsal raphe nucleus is necessary and sufficient for passivity and heightened fear, these being mediated by 5-HT released in regions that proximately control their expression. The detection of uncontrollability is not necessary nor is it sufficient for passivity. This is caused by prolonged exposure to aversive stimulation per se .

Second: DETECT and ACT. When shock is initially escapable , the presence of control is DETECTed. This is accomplished by a circuit involving projections from the prelimbic region of the ventromedial prefrontal cortex (the PL) to the dorsal medial striatum (the DMS), and back. After detection of control, a separate and distinct population of prelimbic neurons are activated that here we call ACT. These neurons project to the dorsal raphe nucleus and inhibit the 5-HT cells that are activated by aversive stimulation, thus preventing dorsal raphe nucleus activation and thereby preventing sensitization of these cells, eliminating passivity and exaggerated fear. So it is the presence of control, not the absence of control, that is detected by prelimbic medial prefrontal circuits, leading to consequent prelimbic-mediated inhibition of stress-responsive brainstem structures such as the dorsal raphe nucleus . When these circuits are inactive the organism reacts passively and fearfully if the aversive event is prolonged.

Third: EXPECT. After the prelimbic-dorsal raphe nucleus ACT circuit is activated a set of changes that require several hours occurs in this pathway and involves the formation of new proteins related to plasticity. This is now a circuit that EXPECTS control. If the rat has previously had control, now even inescapable shock or other uncontrollable stressors activate this prelimbic- dorsal raphe nucleus pathway, which they would not otherwise do. Inescapable shock now activates the sensitized prelimbic- dorsal raphe nucleus pathway, which now operates as an EXPECT circuit. So, inescapable shock is not being detected as uncontrollable, but it is being responded to as if it were controllable . This bias to respond as if the shock was escapable we shall call an EXPECTATION of control. However, it should be clearly understood that this EXPECTATION may not be a cognitive process or entity as psychologists tend to view them. It is a circuit that provides an expectational function, in the sense that it changes or biases how organism's respond in the future as a consequence of the events that occur in the present.

The Neural Circuitry of Learned Helplessness

We now go through the neural circuitry dataset in detail using the PASSIVITY/ANXIETY, DETECT, ACT, and EXPECT terminology both to make the argument more easily understood and because we believe that it is a useful translation from the neural level of analysis to the psychological level of analysis. We are aware that any such translation is merely a hypothesis that can be tested and falsified.

By the mid-1990s it seemed that the neuroscience tools that had become available might allow a more detailed understanding of how the brain produces the behavioral consequences of uncontrollable aversive events. As noted above, a variety of neurotransmitters and receptors had already been implicated, but how the sequelae of inescapable shock are actually caused was obscure.

We state inclusion/exclusion criteria for any adequate neural learned helplessness study at the outset. A study must meet two criteria. First, control over the stressor must be manipulated to determine whether any neural change measured is indeed a consequence of the uncontrollability/controllability of the event. Otherwise, the measured change could be a simple consequence of the stressor per se. There are numerous consequences of exposure to an aversive event that are, in fact, not modulated by control ( Helmreich et al., 1999 ; Maier, Ryan, Barksdale, & Kalin, 1986 ; McDevitt, et al., 2009 ; Woodmansee, Silbert, & Maier, 1993 ). Thus, it is not enough to compare only inescapable shock and non-shocked controls. In the research to be described below, rats are the subject and the response that the ESC subjects can perform to terminate each shock is the turning of a small wheel located on the front of the chamber. Of course, once having established that a particular outcome that follows a particular stressor is indeed a function of controllability, the triadic design may not then be needed in further studies designed to explore the mechanisms by which the incontrollable stressor produces behavioral outcomes. Second, the initial stressor must occur in an environment very different from the test environment since one of the hallmarks of learned helplessness is trans-situationality. When common cues are shared between the first environment and the test environment, processes such as fear conditioning could mediate the behavioral change. For example, there are a large number of reports under the label “biological mechanisms of learned helplessness” that have delivered inescapable gridshocks while the subjects are constrained to one side of a shuttlebox, and then escape learning is tested in that very same shuttlebox. Poor test shuttlebox escape learning could be mediated by fear conditioning to the shuttlebox environment, since freezing is a prominent fear response. Indeed, Greenwood, Strong, and Fleshner (2010) have shown this to be the case. In their studies, manipulations that reduce fear conditioning reduce the shuttle escape deficit when the prior inescapable shocks were administered in the shuttlebox, but not when they were administered outside the shuttlebox.

Passivity/Anxiety and the Dorsal raphe nucleus

It is, of course, difficult to know where to start in a search for the circuitry that mediates learned helplessness. Maier and his colleagues began by reasoning backwards from the behavioral sequelae of inescapable shock. As already noted, many of the behavioral consequences seemed to be captured as either inhibited fight/flight (poor escape, reduced aggression, reduced social dominance) or exaggerated fear/anxiety (decreased social investigation, potentiated fear conditioning, neophobia). By the mid-1990s there was quite a bit known about the neural circuitry that regulates fight/flight and fear/anxiety, and so this information could be used. Most behaviors and emotions are mediated not by a particular structure but rather by a circuit, so the idea was to identify structures that were the most proximal mediators of fight/flight and fear/anxiety, that is, the most efferent part of the circuit closest to the behaviors themselves. The most proximate mediator of fight/flight seemed to be the dorsal periaqueductal gray (dPAG), while the extended amygdala (bed nucleus of the stria terminalis, BNST, together with the amygdala proper) mediated fear/anxiety.

Serotonin (5-HT) and the Dorsal raphe nucleus

So it seemed as if the subjects that received inescapable shock later behaved as if they had inhibited dorsal periaqueductal gray function and exaggerated amygdala/BNST function. There is a structure—the dorsal raphe nucleus – that projects to both, inhibiting one and potentiating the other when it itself is activated. Activation of this structure might then recapitulate the behavioral pattern produced by inescapable shock. The dorsal raphe nucleus sends 5-HT projections to both the dorsal periaqueductal gray and to the amygdala, with 5-HT released in the dorsal periaqueductal gray inhibiting its function and 5-HT in the amygdala potentiating its function (see Graeff, Guimarães, De Andrade, & Deakin, 1996 for review).

Clearly, then, if inescapable shock were to produce a powerful activation of the dorsal raphe nucleus 5-HT neurons and lead to the release of 5-HT in structures such as the amygdala and dorsal periaqueductal gray, then this structure would hold the potential to be a crucial node in any learned helplessness circuit. It would also have to be true that escapable shock does not activate the dorsal raphe nucleus. Of course, it was necessary to investigate whether inescapable shock does not just activate it in some nonselective way, but rather that inescapable shock activates specifically 5-HT neurons. 5-HT containing cell bodies are largely localized to the raphe nuclei, with the dorsal raphe nucleus being the largest and providing much of the 5-HT innervation of forebrain and limbic structures. However, only roughly 1/3 of dorsal raphe nucleus neurons contain 5-HT, and so simply showing generalized activation is not enough. To approach this issue Grahn et al. (1999) labeled 5-HT cells in the dorsal raphe nucleus with an antibody directed at 5-HT. Then, subjects received escapable shock (ESC), yoked inescapable shock (INESC), or no shock, and the expression of markers for neural activation was examined (e.g., the expression of the protein product of the immediate-early gene c-fos) using immunohistochemistry specifically in the cells known to be 5-HT cells. Thus, she was able to show that inescapable shock activated the neurons in the dorsal raphe nucleus that contained 5-HT, and exactly equal escapable shock did not.

The technique of in vivo microdialysis allows the measurement of the levels of 5-HT in discrete brain regions in real-time in live, awake, behaving animals. The results were dramatic. Figure 1 shows the levels of 5-HT within the dorsal raphe nucleus during escapable and inescapable shock. The level of 5-HT within the dorsal raphe nucleus is a measure of dorsal raphe nucleus 5-HT neuronal activity since 5-HT is released within the dorsal raphe nucleus by axon collaterals when the neurons fire. First, baseline levels were measured before the stressors began. Both inescapable shock and escapable shock led to a rapid and large release of 5-HT. This elevated level of 5-HT within the dorsal raphe nucleus was maintained even after the session ended for the inescapable subjects. However, 5-HT dropped precipitously as the escapable subjects learned the instrumental wheel-turn escape response, even though the shocks continued. (We will ask below what made the 5-HT drop as the escapable subjects learned to escape.) Importantly, activation of dorsal raphe nucleus 5-HT neurons also occurs robustly during other essentially uncontrollable stressors such as social defeat ( Amat, Aleksejev, Paul, Watkins, & Maier, 2010 ).

Levels of serotonin (5-HT) in the dorsal raphe nucleus (DRN) measured by in vivo microdialysis before, during, and after exposure to escapable (ESC) and yoked inescapable (IS) tailshocks. Level of 5-Ht is expressed as a percentage of baseline values, and the Baseline, during stress, and Post-Stress is measured in 20 min intervals. IN produced a sustained rise in levels of extracellular 5-HT, while levels during ESC dropped rapidly as the subjects learned the controlling response.

The failure to escape produced by inescapable shock occurs for some number of days (see below for discussion of time course), but the elevation in 5-HT within regions such as the amygdala does not persist for this period of time. How could elevated 5-HT within the amygdala be responsible for behaviors such as passivity and increased anxiety when 5-HT elevations do not persist until testing? A little more information about the dorsal raphe nucleus helps. Receptors of the 5-HT1A subtype are expressed on the soma and dendrites of 5-HT cells within the dorsal raphe nucleus. These are inhibitory autoreceptors – 5-HT binding to these receptors inhibits 5-HT neuronal activity. This 5-HT comes from axon collaterals from neighboring 5-HT cells within the dorsal raphe nucleus. Thus, the activation of a dorsal raphe nucleus 5-HT neuron can lead to the inhibition of its neighbors, and so dorsal raphe nucleus 5-HT activity is under self-restraint. Interestingly, these receptors are desensitized or downregulated by high levels of 5-HT. Thus, 5-HT released within the dorsal raphe nucleus during the strong dorsal raphe nucleus 5-HT activation produced by inescapable shock could desensitize these receptors, leading to a loss of the normal inhibitory restraint on these cells, thereby sensitizing them. Indeed, this is precisely what happens ( Rozeske et al., 2011 ). Inescapable shock, but not exactly equal escapable shock, desensitizes these receptors so that dorsal raphe nucleus5-HT neurons are sensitized for a number of days and to a remarkably large extent. For example, inescapable shock reduces later social investigation of a juvenile, a putative measure of anxiety ( Christianson, Paul, et al., 2008 )). Placing a juvenile into an adult's rat cage, as is done in this test, produces no increase in 5-HT activity at all in control subjects. However, the mere presence of a juvenile leads to a large increase in 5-HT within the amygdala in a subject that has experienced inescapable shock, but not escapable shock previously ( Christianson et al., 2010 ). Of course, the desensitization of 5-HT1A receptors is not permanent, and recovers to normal within 3 days ( Rozeske et al., 2011 ). Importantly, behavioral sequelae of IS such as escape deficits and anxiety also persist for just this period of time ( Maier, 2001 ).

Dorsal raphe nucleus Activation is Necessary and Sufficient for Passivity/Anxiety

The fact that uncontrollable stressors differentially activate and sensitize dorsal raphe nucleus 5-HT neurons does not mean that this process is either necessary or sufficient to produce the passivity and anxiety that follows inescapable shock. Three strategies have been adopted to determine necessity.

• Blockade of the dorsal raphe nucleus activation produced by inescapable shock. Here, activation of the dorsal raphe nucleus during inescapable shock was prevented by either lesion ( Maier et al., 1993 ; Will et al., 2004 ) or microinjection of pharmacological agents that prevent dorsal raphe nucleus 5-HT activation ( Maier, Grahn, & Watkins, 1995 ; Maier, Kalman, & Grahn, 1994 ). These treatments all prevented inescapable shock from producing its usual poor escape and heightened anxiety, and these subjects behaved as did non-shocked controls.
• Prevention of the desensitization of 5-HT1A receptors on dorsal raphe nucleus5-HT neurons produced by inescapable shock. Here an antagonist to the 5-HT1A receptor was microinjected into the dorsal raphe nucleus during inescapable shock, and as above these subjects behaved later as if they had not received the inescapable shock.
• Blockade of 5-HT receptors in the dorsal raphe nucleus target regions during later testing. The argument is that failure to escape and increased anxiety occur because excessive 5-HT is released in critical target structures such as the amygdala during behavioral testing. Thus, blocking the receptors to which the 5-HT binds should eliminate the passivity and increased fear that typically occurs after inescapable shock. Indeed, microinjection of 5-HT2C antagonists directly into these structures does block the passivity and increased anxiety ( Christianson et al., 2010 ; Strong et al., 2011 ).

Sufficiency of Dorsal raphe nucleus Activity for Passivity/Anxiety

With regard to sufficiency, simply activating the dorsal raphe nucleus by microinjecting agents into the dorsal raphe nucleus that activate 5-HT neurons should produce the same passivity and anxiety as does inescapable shock. Although there is less work directed at this issue, this appears to be the case. Direct activation of the dorsal raphe nucleus by microinjection of the GABA antagonist picrotoxin or the benzodiazepine receptor antagonist beta-carboline both produce the typical behavioral outcomes that are produced by inescapable shock ( Maier, Grahn, Maswood, & Watkins, 1995 ; Short & Maier, 1993 ).

Learning: How and What does the Dorsal raphe nucleus Know?

The work above indicates that dorsal raphe nucleus 5-HT neurons are selectively activated if the shock is inescapable, and that this activation is necessary and sufficient to produce passivity and anxiety. But the key question is why the dorsal raphe nucleus responds only if the shock is inescapable . The most obvious option is that the dorsal raphe nucleus DETECTS the uncontrollability of the shock. To do so the dorsal raphe nucleus would have to extract the conditional probability of the shock offset given that the wheel turn or some other escape response occurs, and the conditional probability of the shock offset occurring in the absence of those responses, and compare these two probabilities. When the probabilities are equal the shock is uncontrollable. However, to do this, the dorsal raphe nucleus would require inputs informing it whether the motor responses have occurred and whether the shock is present or not, but the dorsal raphe nucleus does not receive these types of somatomotor and somatosensory inputs.

The next possibility is that the dorsal raphe nucleus receives greater excitatory inputs during inescapable than during escapable shock, thereby leading to more activation with inescapable shock. Indeed, a number of inputs to the dorsal raphe nucleus during stress have been discovered, but none provide more excitatory input during inescapable shock than during escapable shock. For example, recall that Weiss and his colleagues ( Weiss & Simson, 1988 ) found that inescapable shock activates locus coeruleus norepinephrine (NE)-containing neurons. These project to the dorsal raphe nucleus, and consistent with the Weiss work, blockade of NEreceptors in the dorsal raphe nucleus with a microinjected antagonist during inescapable shock eliminated the passivity and anxiety ( Grahn et al., 2002 ). However, both escapable and inescapable shock produced exactly equal levels of locus coeruleus NE activation ( McDevitt et al., 2009 ). That is, although locus coeruleus input to the dorsal raphe nucleus was required for learned helplessness, both inescapable and escapable shock led to equivalent inputs to the dorsal raphe nucleus . Moreover, a similar pattern was found for several other inputs to the dorsal raphe nucleus occurring during the shock. So, the conclusion is that the dorsal raphe nucleus does not receive any heightened excitation from inescapable shock relative to escapable shock.

Learning: The Ventromedial Prefrontal Cortex does DETECT and EXPECT

In sum, a number of inputs to the dorsal raphe nucleus, using a number of different transmitters, was necessary to produce learned helplessness behaviors, but these inputs did not discriminate inescapable from escapable shock. If inescapable shock produces a much greater activation of dorsal raphe nucleus 5-HT neurons than does escapable shock, but both provide equivalent excitatory input , then there is only one obvious possibility left—the presence of control must somehow inhibit dorsal raphe nucleus 5-HT neurons that would otherwise be activated by shock per se without regard to controllability . The computational complexity of detecting the presence of control suggests a cortical process, and the dorsal raphe nucleus receives virtually all of its cortical input from the prelimbic region (PL) of the ventromedial prefrontal cortex (vmPFC) ( Peyron, Petit, Rampon, Jouvet, & Luppi, 1997 ; Vertes, 2004 ). Importantly, electrical stimulation of the neurons that descend from the prelimbic area to the dorsal raphe nucleus inhibits dorsal raphe nucleus neuronal activity. Although these descending neurons are glutamatergic and so excitatory, they synapse preferentially on GABAergic interneurons in the dorsal raphe nucleus that inhibit the 5-HT cells (see Figure 2 for a cartoon). This arrangement leads to the hypothesis that escapability (control) is DETECTed by the ventromedial prefrontal cortex, and that the ventromedial prefrontal cortex then ACTs to inhibit shock-induced dorsal raphe nucleus activation . The dorsal raphe nucleus is a site of convergence that sums inputs from a number of structures themselves activated by shock ( Figure 3 ). One idea is that these different inputs encode different aspects of aversive events, and so the more that are activated the more serious the threat. The dorsal raphe nucleus is important because it has this integrative function, and in turn projects to structures that are the proximate mediators of passivity/anxiety, our shorthand for the various behavioral and mood changes that follow inescapable shock. Thus, the dorsal raphe nucleus plays a role with respect to passivity somewhat analogous to that of the central nucleus of the amygdala in mediating fear. However, the dorsal raphe nucleus 5-HT neurons are under the inhibitory control of the prelimbic region of the ventromedial prefrontal cortex, and the detection of escapable shock activates this top-down inhibition of the dorsal raphe nucleus. We will return to a discussion of how this detection is accomplished.

Schematic depiction of ventromedial medial prefrontal cortex (vmPFC) dorsal raphe nucleus (DRN) interactions. Excitatory glutamatergic projections from the vmPFC synapse onto inhibitory GABAergic interneurons within the DRN that inhibit the serotonin (5-HT) neurons.

Schematic depiction of the proposed model. Serotonin (5-HT) neurons in the dorsal raphe nucleus (DRN) integrate stress-responsive inputs that encode different aspects of a stressor and then activate brain regions that are the proximate mediators of the behavioral effects of uncontrollable stress. Glut=glutamate; vmPFC=ventral medial prefrontal cortex; GABA=gamma aminobutyric acid; 5-HT=serotonin; DRN=dorsal raphe nucleus; habenula=habenula; LC=locus coeruleus; BNST=bed nucleus of the stria terminalis; PAG=periaqueductal gray; amygdala=amygdala; N. Acc.=nucleus accumbens.

Does the ventromedial prefrontal cortex actually regulate dorsal raphe nucleus activity and passivity as specified by this model ( Figure 3 )?

First, does the presence of escapable shock, but not inescapable shock, activate ventromedial prefrontal cortex neurons that project to the dorsal raphe nucleus? It would be easy to administer escapable shock, yoked inescapable shock, or no shock treatment and then determine whether the ventromedial prefrontal cortex is selectively activated by the escapable shock. However, most of the cells in the ventromedial prefrontal cortex have nothing to do with projections to the dorsal raphe nucleus, and so more is needed to indicate that the specific ventromedial prefrontal cortex pathways that project to the dorsal raphe nucleus are activated by escapable shock. To answer this question Baratta et al. (2009) microinjected a retrograde tracer into the dorsal raphe nucleus. Retrograde tracers are taken up by axon terminals within the dorsal raphe nucleus and transported back to the neuronal cell bodies. This labels all cell bodies in the ventromedial prefrontal cortex that project to the dorsal raphe nucleus. Baratta et al. (2009) then later administered escapable shock, inescapable shock, or no shock. It was then only necessary to determine whether the cells that were labeled as projecting from the ventromedial prefrontal cortex to the dorsal raphe nucleus were activated, which was done by examining within these labeled neurons the expression of markers of neuronal activation such as the immediate-early gene c-fos . Indeed, escapable shock but not exactly equal inescapable shock, increased c-fos protein in the labeled projecting neurons.

Second, is activation of this pathway necessary for escapable shock to reduce dorsal raphe nucleus activation and block the passivity and anxiety usually produced by inescapable shock? To answer this question Amat et al. (2005) inactivated the ventromedial prefrontal cortex-to-dorsal raphe nucleus pathway during the experience of escapable shock, inescapable shock, or no shock. This was done by microinjecting a pharmacological agent into the prelimbic area that inhibits the glutamatergic pyramidal neurons that project to the dorsal raphe nucleus (see Figure 4 ). The results were dramatic. Although the subjects with control learned the escape response perfectly, this learning was no longer protective —the dorsal raphe nucleus was activated as if the tailshocks were actually inescapable, and the subjects showed the passivity and heightened anxiety typical of exposure to inescapable shock. That is, inactivating the ventromedial prefrontal cortex-to-dorsal raphe nucleus pathway turned an animal with control into an animal without control.

Schematic depiction of experimental strategy to determine whether activation of the ventromedial prefrontal cortex (vmPFC) to dorsal raphe nucleus (DRN) pathway is necessary for the presence of behavioral control to be protective. Blockade of the vmPFC to DRN pathway would prevent behavioral control from activating the inhibitory GABAergic cells that control the 5-HT neurons.

Third, is activation of this pathway sufficient for control to reduce dorsal raphe nucleus activation and block the passivity typically produced by inescapable shock? That is, does the organism actually need to escape at all, or is the mere activation of this pathway during the shock enough? To answer this question Amat, Paul, Watkins, and Maier (2008) activated this pathway directly with a microinjected pharmacological agent during the experience of inescapable shock. Now the dorsal raphe nucleus was inhibited as if the stressor was escapable, which it was not, and passivity was prevented. That is, activating the ventromedial prefrontal cortex-to-dorsal raphe nucleus pathway turned an animal without control into an animal with control.

Detection of control

So the presence of control activates descending inhibition of shock-induced dorsal raphe nucleus activation and thereby blocks passivity and anxiety. However, this does not mean that control is necessarily detected by the ventromedial prefrontal cortex in isolation, or by the ventromedial prefrontal cortex at all. Control could be detected by a different circuit, with this information then conveyed over to the ventromedial prefrontal cortex.

The clue to how Maier and his students proceeded with this issue came from the literature on the neural mechanisms underlying appetitive instrumental learning—for example a rat learning to press a lever for food. The history of psychology witnessed a debate as to whether instrumental learning involves the formation of a Stimulus-Response habit or instead a Response-Reinforcer expectancy. Neuroscience research indicates that each can take place and each involves different neural systems ( Balleine & O'Doherty, 2010 ). One system, called the “act/outcome” system, is sensitive to the contingency between response and reinforcer. Contingency is “the difference between the probability of obtaining a target reward (r) given that a specific action (a) is performed and the probability of gaining the reward in the absence of the action” ( Liljeholm, Tricomi, O'Doherty, & Balleine, 2011 , p. 2474). The act/outcome system leads to “flexible” learning, and it is sensitive to contingency changes in the reward. A second system, the “habit” system, is a mere habit that is not sensitive to contingency but only to the temporal pairing between response and reward, and it produces inflexible learning that is not sensitive to changes in the contingency of the reward ( Balleine & Dickinson, 1998 ). Importantly, the act/outcome system involves a corticostriatal circuit consisting of the prelimbic area within the ventromedial prefrontal cortex and the posterior dorsal medial striatum (DMS), while the habit system has no prefrontal cortical involvement, but instead involves the sensorimotor cortex and the dorsal lateral striatum (DLS). Thus, lesion, NMDA receptor blockade, and inactivation of either the prelimbic area or the dorsal medial striatum prevents contingency sensitive act/outcome learning. Responses can be learned, but only the habit system is then used, and so the learning is insensitive to contingency ( Shiflett & Balleine, 2011 ).

Interestingly, this definition of instrumental contingency is identical to the definition of control that Maier and Seligman (1976) provided, although Maier and Seligman were referring to shock rather than food. Maier and Seligman defined control as being present whenever the conditional probability of the outcome (shock termination) after some response is different from the conditional probability of the outcome in the absence of that response, an identical formalism that provided for contingency in the appetitive instrumental learning literature 40 years later.

All this suggested that perhaps DETECTion of control over shock is done by a circuit involving the prelimbic area and the dorsal medial striatum, just as is instrumental appetitive contingency learning. As would be predicted, Amat et al. (2014) found that escapable shock, but not inescapable shock activates the contingency-sensitive dorsal medial striatum, but not the habit-oriented contingency-insensitive dorsal lateral striatum. The impact of inactivating the dorsal medial striatum during the experience of escapable and inescapable shock was even more intriguing. First, inactivating the dorsal medial striatum did not interfere with the learning and performance of the escape response. This suggests that the rats could use the “dumber” habit system to acquire and perform the escape response. Dramatically, even though the escapable subjects performed the controlling escape response perfectly, this was not protective against passivity/anxiety later. So when the habit system and not the contingency-sensitive system is used, detecting control seems to be absent. That is, the dorsal raphe nucleus was activated as if the shocks were uncontrollable and passivity/anxiety followed. Thus, it is not turning the wheel and actually escaping the shock by wheel turning that is necessary to prevent later passivity, but rather the detection of escapability by the prelimbic-dorsal medial striatum act/outcome system . As this conclusion also predicts, inactivating the dorso lateral striatum and the habit system did not reduce the protective effects of escapability. It might be noted that the precise mechanism by which the prelimbic-dorsomedial striatum circuit does the “detecting” is not known.

In sum, the prelimbic region of the ventromedial prefrontal cortex is involved in two separable functions-the DETECTion of control in a circuit with the dorsal medial striatum and then ACTing to inhibit the dorsal raphe nucleus (see Figure 5 ). Is it the same prelimbic neurons that are involved in both detection of contingency and ACTing on this information by transmitting it to the dorsal raphe nucleus and inhibiting it? To answer this question M. Barratta (unpublished) in Maier's group microinjected one color retrograde tracer in the dorsal medial striatum and a differently colored retrograde tracer into the dorsal raphe nucleus. These tracers were transported backwards along the neurons to the cell bodies of the neurons in the prelimbic area that project to these structures. If the same prelimbic neurons project to both regions then both colors should be present in the same cell bodies in the prelimbic area. There was no colocalization at all, indicating that these are separate populations of prelimbic neurons. Thus, DETECT escapability and ACT to pass this information that then inhibits the dorsal raphe nucleus are subserved by different populations of ventromedial prefrontal cortex cells and so are truly different functions.

Schematic depiction of the role of the prelimbic cortex (PL) in mediating the impact of behavioral control. Separate systems are involved in the detection of control, and then acting on this detection. The detection circuit involves bidirectional flow between the dorsomedial striatum (DMS) and the prelimbic cortex while the action circuit consists of neurons that project from the PL to the dorsal raphe nucleus (DRN).

Immunization and EXPECTation

Initial exposure to escapable shock prevents or reduces the passivity/anxiety induced by later inescapable shock, a phenomenon we called immunization ( Maier et al., 1969 ). Two features of immunization are essential. First, it is quite enduring , but perhaps not permanent. Second, it is trans-situational and so inescapable shock in one situation blocks the passivity/anxiety caused by even stressors that do not involve shock in different situations. For example, Amat et al. (2010) reported that experience with escapable shock blocked the passivity in shuttle escape and also blocked the reduced social investigation (anxiety) produced by social defeat occurring seven days later. Social defeat involves placing the experimental subject together with a larger and aggressive dominant subject. The experimental subject inevitably loses and adopts defeat postures, and so there is a strong element of uncontrollability. Here there is no shock at all, no restraint, the defeat is conducted on a different floor of the building by different experimenters, and yet escapable shock immunized against the effects of defeat. As would be expected, social defeat also increased dorsal raphe nucleus 5-HT activity, and this increase was prevented by the prior escapable shock ( Amat et al., 2010 ).

Why does the inescapable shock (or defeat) fail to activate dorsal raphe nucleus 5-HT neurons and thus produce the typical passivity/anxiety if the organism has first experienced control over shock? Given the circuitry above, perhaps the uncontrollable shock (or defeat) now activates the prelimbic-to dorsal raphe nucleus inhibitory pathway, even though without the prior immunizing experience of escapable shock it would not do so. To determine whether this is the case, Baratta et al. (2009) microinjected a retrograde tracer in the dorsal raphe nucleus in order to label prelimbic neurons that project to the dorsal raphe nucleus. Recall that escapable shock but not inescapable shock activates these labeled cells, as assessed by examining activation markers such as c-fos in these labeled neurons. Dramatically, inescapable shock now does activate these cells as if the inescapable shock was escapable shock – if the organism had experienced immunizing control seven days earlier! Furthermore, when these prelimbic neurons were inactivated during the inescapable shock via the microinjection of inhibitory pharmacological agents, immunization no longer occurred ( Amat, Paul, Zarza, Watkins, & Maier, 2006 ).

Thus, the experience of escapable shock (control) produced a specific and persistent change in the prelimbic-dorsal raphe nucleus circuit that led to the inhibition of the dorsal raphe nucleus and prevented passivity in response to even uncontrollable stress. The obvious possibility is that the activation of this pathway that occurs during escapable shock is sufficient to produce the persistent change. To test this idea Amat et al. (2006) activated this pathway directly by microinjecting a pharmacological agent with no actual escapable shock present, but this did not produce the persistent pathway change or produce immunization. They then reasoned that perhaps it is the joint activation of this pathway and the occurrence of the shock that is critical. To test this, the prelimbic-dorsal raphe nucleus pathway was activated pharmacologically during the occurrence of inescapable shock , the uncontrollable form of the stressor. Remarkably, now immunization occurred. That is, inescapable shock produces immunization as long as the prelimbic pathway is activated during shock.

How can this be understood? It is known that without prior escapable shock activation of the prelimbic-dorsal raphe nucleus ACT pathway requires the detection of control by the prelimbic-dorsal medial striatum DETECT circuit. We suspect that it also requires the presence of a potent aversive event, as there would be no reason to inhibit the dorsal raphe nucleus if there were not an aversive event present. This assertion could be tested, although the appropriate experiment has not yet been done. Plasticity, or increased connectivity between neurons at a synapse, typically occurs when both are activated together, as they say, “neurons that fire together wire together”. Thus, the joint occurrence of shock and control might induce increased connectivity so that later just the presence of the shock, without control, is sufficient to activate the pathway. Recent evidence supports this idea: 1) The development of persistent increases in connectivity requires the production of new proteins in the cells in question, and blockade of new protein synthesis in the prelimbic area after the escapable shock experience prevents immunization ( Amat et al., 2006 ). That is, even though the subjects exert control and the prelimbic area is activated, immunization only happens if new proteins can be formed. Importantly, control still blunts the impact of the stressor being experienced, but longer-term immunization is eliminated; 2) The production of particular proteins, called plasticity proteins, is required for long term-increases in connectivity. Increases in these particular proteins (e.g., phosphorylated extracellular signal-regulated kinase) are indeed induced in the prelimbic region of theventromedial prefrontal cortex by escapable shock ( Christianson et al., 2014 ); 3) Inhibitors of just these plasticity proteins prevent immunization when microinjected in the prelimbic area ( Christianson et al., 2014 ); and 4) Direct electrophysiological measurement of projecting prelimbic neurons indicates that escapable shock, but not inescapable shock increases their excitability ( Varela, Wang, Christianson, Maier, & Cooper, 2012 ). We conclude from this that the prelimbic-dorsal raphe nucleus ACT pathway can be modified over several hours after the joint experience of control and aversive stimulation, to respond to stressors in general as if they were controllable, and this is compatible with the idea that this altered pathway subserves the EXPECTation that shock will be controllable in new aversive situations. Thus, the same prelimbic-dorsal raphe nucleus pathway that operates as ACT can later operate as EXPECT.

The ventromedial prefrontal cortex projects to many structures other than the dorsal raphe nucleus. The amygdala is especially interesting in this regard. The role of the amygdala in fear and conditioned fear is well known. Briefly, the association between a stimulus predicting shock and the shock forms in basolateral regions of the amygdala. From there the information passes to the central nucleus of the amygdala, which in turns projects to the regions that control the behaviors and physiological responses that are the symptoms of fear ( Davis, Rainnie, & Cassell, 1994 ; LeDoux, 2003 ; Maren & Quirk, 2004 ). For example, the central nucleus of the amygdala projects to regions of the periaqueductal gray that produce freezing, a behavioral component of conditioned fear. Both the prelimbic and the infralimbic region of the ventromedial prefrontal cortex project to parts of the amygdala. Of special note, the infralimbic region sends excitatory glutamatergic projections to a region of the amygdala known as the intercalated cell region. The cells in this region are GABAergic and project to and inhibit the central nucleus of the amygdala ( Berretta, Pantazopoulos, Caldera, Pantazopoulos, & Pare, 2005 ). Thus, stimulation of the infralimbic region should inhibit fear expression, and it does ( Sierra-Mercado, Padilla-Coreano, & Quirk, 2011 ). Since the prelimbic-dorsal medial striatum circuit DETECTS control, and since the prelimbic communicates with the infralimbic region of the ventromedial prefrontal cortex, Baratta et al. (2007) wondered whether the experience of control over an aversive event might reduce later fear in a different situation. Thus, subjects were exposed to escapable shock or yoked inescapable shock in the wheel-turn apparatus and given fear conditioning in standard conditioning chambers seven days later. Inescapable shock potentiated later fear conditioning, a well-known phenomenon ( Rau, DeCola, & Fenselow, 2005 ). It would not have been surprising if initial control merely prevented this potentiating effect, but it did more than that: Instead prior escapable shock actually retarded fear conditioning and facilitated fear extinction. This indicated an EXPECTation of control over shock. Moreover, these effects of prior control depended on the ventromedial prefrontal cortex ( Baratta, Lucero, Amat, Watkins, & Maier, 2008 ), showing that this structure exerts top-down inhibition of more than just the dorsal raphe nucleus, and the limits of this arrangement await further exploration.

Neurobiology of Human Control

Although there is a long history of research investigating the controllability dimension in humans, studies using methods that allow the measurement of neural activity are quite recent and few in number. A number of studies employing painful stimuli have found that providing control, or inducing perceived control, reduces the experienced intensity of the painful stimulus. Moreover, perceived control in these pain studies increases ventromedial prefrontal cortex activity ( Salomons, Johnstone, Backonja, & Davidson, 2004 ). In the only relevant triadic design of which we are aware, Kerr, McLaren, Mathy, and Nitschke (2012) used exposure to snake videos to subjects with snake phobias. Each trial began with an anticipation period of variable duration in which a cue signaled that a snake video or a neutral fish video might follow. A second cue indicated whether the subject would or would not have control over whether the video would occur on that trial. After a variable period of time a target then occurred and the subject was instructed to press it as rapidly as possible. The video or a fixation point then appeared. On a controllable trial subjects were told that if they responded fast enough the fixation point rather than the video would appear, but if they were too slow they would see the video. On uncontrollable trials the subjects were told that no matter of how quickly they pressed, the video and the fixation point would each occur half the time, but subjects were asked to press as fast as possible anyway. However, the speed required on controllable trials was adjusted so that the subjects succeeded about half the time in avoiding the video, and so the actual frequencies on the uncontrollable trials was equated to this frequency. Thus, the controllable and uncontrollable trails were exactly yoked, as in animal studies. As expected, perceived control over the snake presentation reduced anticipatory anxiety on snake trials. Importantly, there was one condition that selectively excited ventromedial prefrontal cortex activity – snake controllable trials. Control did not increase ventromedial prefrontal cortex activity on neutral fish trials, even though the subjects pressed. Ventromedial prefrontal cortex activity was higher on controllable snake trials than in any of the other conditions. Finally, there was a negative relationship between ventromedial prefrontal cortex and amygdala activity on snake trials. These findings provide some support for generalizing the animal data reviewed above to humans.

Contrasting Psychological and Neural Explanations of Learned Helplessness

We believe that the neural explanations strongly inform the psychological explanations. We suspect that the learned helplessness work now provides a good, generalizable example of the complementarity between neural and psychological explanations. In the present case, the detailed knowledge concerning neural processes enabled the testing and major revision of the original psychological theory of learned helplessness—refinements that could not have happened without knowing the neural circuitry (examples below). On the other hand, the neural work would likely never have been done without the original behavioral work and psychological theorizing. Recall that the phenomenon that began this line of work was that exposure to aversive Pavlovian fear conditioning leads to later failure to learn instrumental escape/avoidance responses ( Leaf, 1964 ). It was behavioral work and psychological theorizing that led to the isolation of behavioral control/lack of control as being the key feature of the Pavlovian conditioning that led to the failure to learn, and without this work there would not have been neuroscientific research directed at understanding the mechanisms that underlie controllability effects. The neuroscience circuitry work then clarified numerous issues (see below), but then translation back to psychological concepts also seems useful. As will be discussed below, the translation back to the psychological level enables the neuroscience work to potentially inform clinical practice.

Hypothesis Testing

First, Maier's group was able to test hypotheses that did not seem testable at the psychological level. The psychological theorizing concerning learned helplessness flowed from the triadic design that compared subjects with no control and those with control. The basic result was that the subjects without control later revealed passivity and a number of other behavioral changes, while those with control did not and appeared to be similar to non-shocked controls. Given this pattern we inferred that detecting and expecting a lack of control was the active ingredient. The non-difference between the zero group and the escapable shock group led us to believe that organisms expected controllability as the basic “default option”. Alternatively, it has been argued (e.g., Minor, Dess, & Overmier, 1991 ) that the reverse could be true, that stressors per se have deleterious effects, and that these effects could then be blocked when control was added as the active ingredient. However, it was difficult to separate these two possibilities with behavioral experiments, and the idea that uncontrollability was learned remained the dominant view.

The neural work allowed the testing of whether control is the active ingredient and lack of control is the default option, rather than the other way around as the psychological theory claimed. There are several key points. The neural evidence strongly suggests that activation and sensitization of the dorsal raphe nucleus leads to the passivity and anxiety characteristic of learned helplessness. Of course, inescapable shock produces a greater activation of the dorsal raphe nucleus than does controllable shock. But there were two obvious possibilities as to why: Is this differential activation because inescapable shock provides more excitatory input to the dorsal raphe nucleus than does escapable shock, or is it because escapable shock provides more inhibitory input to the dorsal raphe nucleus? Either would produce differential activation of the dorsal raphe nucleus by inescapable versus escapable shock and of course, both could be true. But the neural data are clear. Inescapable shock does not provide more excitatory input—both forms of shock produce equal excitation of the dorsal raphe nucleus. However, when shock is escapable this is DETECTed by the ventromedial prefrontal cortex-dorsal medial striatum circuit, and then the ventromedial prefrontal cortex ACTs, sending inputs to the dorsal raphe nucleus that inhibit it, thereby turning off the activation produced by shock per se . That is, there is nothing in the brain that is selectively turned on by a lack of control, only something that turns things off when there is the presence of control. So, aversive events per se (either controllable or uncontrollable) excite the dorsal raphe nucleus, but control over stress actively turns this off.

The reader may wonder why then in all the initial helplessness experiments the previously nonshocked group and the previously escapably shocked group performed equally well in shuttlebox escape. Recall that passivity/anxiety is explained by 5-HT accumulation during the testing in projection regions of the dorsal raphe nucleus that mediate these behaviors. If control leads to sensitization of the prelimbic-dorsal raphe nucleus pathway (EXPECT), then 5-HT activity should be inhibited from the start during shuttlebox escape testing in this group, but not in the non-shocked controls. It is easy to see why the inescapably shocked group should perform more poorly than controls—the dorsal raphe nucleus 5-HT neurons are sensitized in these subjects at the start of testing and so the aversive stimulus in the shuttlebox test (the gridshock) would lead to large and rapid 5-HT activation and consequent passivity/anxiety. But, if control leads to EXPECT (sensitized prelimbic-dorsal raphe nucleus inhibition), why should the escapably shocked subjects not perform better than controls that had not been previously stressed and so do not have EXPECT? The answer likely lies in an accidental feature of shuttlebox escape learning—it is learned very rapidly. Indeed, rodents escape with almost asymptotically fast latencies by the second or third trial (e.g., Grahn, Watkins, & Maier, 2000 ). This is likely because running is elicited as a species specific defense response ( Bolles & Fanselow, 1980 ) on the very first trials. It is important to understand that 5-HT in response to aversive stimulation accumulates gradually across trials, and so the non-shocked controls learn control before 5-HT levels that could induce passivity have accumulated in regions such as the dPAG and striatum. This DETECTion of control, would, of course, inhibit the dorsal raphe nucleus. Even if there were a slight difference in 5-HT, the shuttle response is learned so rapidly that there is a ceiling effect. This argument would suggest that in tasks in which the non-shocked control is not at ceiling a difference between the previously escapably shocked and non-shocked controls might emerge, and this appears to be the case ( Baratta et al., 2007 ).

A second theoretical advance came from the neural circuitry: We know that the part of the brain that DETECTs control is a circuit formed by the prelimbic area of the ventromedial prefrontal cortex and the dorsal medial striatum. When this system was inactivated so that control/lack of control information could not be detected and subjects were exposed to escapable shock or inescapable shock, the rats reacted to the shock as if it were inescapable – both in terms of passivity/anxiety and of neurochemistry. The data showed that all the animals, regardless of whether they had an escape response that they learned perfectly, acted later as if the stressor had been inescapable. That is, if the control detecting circuit was taken off line, all animals acted as if the shock was inescapable whether the animal actually was able to escape the shock or not. This suggests that if the DETECT control circuit is absent the animal invariably reverts to the default of helplessness following exposure to any prolonged stressor.

The neural circuitry also allowed the test of a competing theory of learned helplessness. It had been argued that the feedback from the escape response becomes a Pavlovian inhibitor of fear, a safety signal that reduces the total fear experienced and that it is this excess fear—if unreduced – that produces passivity (see above). There is no question that the presence of safety signals that predict a period of time free from shock can reduce the behavioral impact of aversive events. With knowledge of the underlying neural circuitry it became simple to ask whether safety signals blunt the impact of stressors via the same or a different mechanism. As discussed above, the escape response exerts its behavioral effects by activating ventromedial prefrontal cortex top-down inhibition of brainstem and limbic stress-responsive structures. It is straightforward to ask whether the protective effects of safety signals also requires the ventromedial prefrontal cortex, and the answer is no . For example, ventromedial prefrontal cortex lesions eliminated the ability of behavioral control to blunt the passivity and fear caused by inescapable shock, but these lesions did not even reduce the passivity and fear blunting impact of safety signals ( Christianson, Benison, et al., 2008 ). Instead, safety signals had their impact via the insular cortex and insular cortex lesions eliminated the protective effects of safety signals. However, insular lesions did not reduce the passivity blunting effects of having an escape response, thereby demonstrating a double dissociation ( Christianson, Benison, et al., 2008 ). Thus, control cannot be reduced to safety. This does not mean that safety signals are not stress-blunting, nor that safety signals do not have clinical uses, but only that stressor control and safety signals exert their effects via different neural mechanisms.

Another theoretical advance provided by the neural circuitry concerns understanding how experiences of control alter how organisms respond to future events. If the rats first experience is with escape the organism is immunized and reacts to subsequent stressors in new situations as if they are escapable. This suggests that the rat EXPECTs that shock will be escapable in the new situation and that plasticity in the prelimbic-dorsal raphe nucleus subserves this expectation and inhibits the dorsal raphe nucleus, thus blocking learned helplessness.

In addition to theory testing, knowledge of the underlying circuitry explained a number of learned helplessness phenomena that were simply mysteries at a psychological level. Here are two examples.

Time course of learned helplessness

The passivity produced by inescapable shock is transient, lasting for only a few days after the inescapable shock. If the behavioral effects of inescapable shock are mediated by the learned expectation that active responding will not produce relief, the original idea, then why this time course? No satisfactory explanation could be conjured at the psychological level. The neuroscience work predicts the time course. The passivity occurs because excessive 5-HT is released in projection regions of the dorsal raphe nucleus, and this occurs because dorsal raphe nucleus 5-HT neurons have become sensitized due to the desensitization of 5-HT1A receptors on the soma and dendrites of these cells. Thus, these behavioral changes should exist only as long as the receptors remain desensitized, which proved to be for only a few days ( Rozeske et al., 2011 ).

The hypothalamo-pituitary-adrenal (HPA) response

The hypothalamo-pituitary-adrenal response begins with the production of corticotropin releasing hormone (CRH) in the paraventricular nucleus of the hypothalamus. Corticotropin releasing hormone travels to the anterior pituitary where it stimulates the production and release of adrenocorticotrophic hormone (ACTH) into the bloodstream. Adrenocorticotrophic hormone in turn stimulates the production and release of glucocorticoids (corticosterone in the rat, cortisol in humans) from the adrenal cortex into the blood. The hypothalamo-pituitary-adrenal response is often considered to be the hallmark of the bodily reaction to stressors, so it would be natural to assume that inescapable shock would produce a larger hypothalamo-pituitary-adrenal response than equated escapable shock. But, at least in the rodent, it does not (see Dess, Linwick, Patterson, Overmier, & Levine, 1983 for different results in dogs). In the rodent, the corticosterone rise is not greater or more prolonged ( Helmreich et al., 2012 ; Maier et al., 1986 ), the adrenocorticotrophic hormone rise is not greater or more prolonged ( Maier et al., 1986 ), nor is the increase in corticotropin releasing hormone in the hypothalamus larger ( Helmreich et al., 1999 ). This unexpected finding has been inexplicable by psychological theory or behavioral considerations. Why should control modulate passivity, fear, and the neurochemical impact of a stressor but not the hypothalamo-pituitary-adrenal response? It follows from the circuitry. Retrograde and anterograde tracing studies indicate that the dorsal raphe nucleus does not send a major projection to the paraventricular nucleus of the hypothalamus, and perhaps none at all ( Larsen, Hay-Schmidt, Vrang, & Mikkelsen, 1996 ). Thus, the dorsal raphe nucleus is not a major source of the hypothalamo-pituitary-adrenal activation during stress ( Herman & Cullinan, 1997 ). The presence of control could reduce or inhibit paraventricular activation only if the structures that DETECT control project to the paraventricular nucleus. There is a pathway from the ventromedial prefrontal cortex to the paraventricular nucleus, but it goes through a relay in the bed nucleus of the stria terminalis, rather than directly ( Radley & Sawchenko, 2011 ). We ( Baratta (2015 ) thus utilized retrograde tracing techniques combined with the assessment of activation markers to determine whether the projections from the ventromedial prefrontal cortex to the bed nucleus of the stria terminalis are controllability-sensitive, and they are not. Thus, we would expect that control would not modulate the HPA axis response to stress because the paraventricular nucleus is not informed about controllability by the ACT circuit.

What Did Original Learned Helplessness Theory Get Right and What Did It Get Wrong?

On the positive side, we found that as the original theory claimed, organisms are sensitive to the dimension of control, and this dimension is critical. However, the part of the dimension that is detected or expected seems now to be the presence of control, not the absence of control . It also appears that the passivity and increased anxiety that follows uncontrollable stressors for several days is not produced by any expectancy at all, but rather is an unlearned reaction to prolonged aversive stimulation that sensitizes a specific set of neurons. Importantly, the presence of control aborts this process. However, expectancy does play a role, but it does in the immunization process. Here, an expectancy of control does blunt the impact of subsequent stressors. Clearly, the neurobiological data are at odds with the theory we held fifty years ago. When we first found that dogs given inescapable shock later failed to learn to escape in a shuttlebox, but that dogs given exactly equated escapable shock later escaped normally, the ideas that we developed were shaped by thinking of what might be most adaptive for dogs, rats and people. We reasoned that active coping is generally best because this would minimize exposure, and so we assumed that organisms would initially expect control to be possible. If the stressor proved to be uncontrollable, organisms would then learn this and expect it to be true in related situations in the future, with this expectation of uncontrollability undermining trying active coping. However, the neural basis of inescapable and escapable shock effects does not support this general schema. Instead, the presence of control seems to be the active ingredient, leading to the inhibition of threat-induced changes in limbic and brainstem structures.

Perhaps this counterintuitive arrangement becomes more intelligible if one considers our phylogenetic ancestors. In primitive organisms threats engage defensive reflexes ( Walters & Erickson, 1986 ). However, these reflexes are energy intensive, and so if unsuccessful it might be adaptive to inhibit them and conserve energy for use in physiological adjustments that promote survival, such as altering the responsivity of the immune system to be better able to fight any infection or wound that might occur after an attack ( Frank, Watkins, & Maier, 2013 ). Primitive organisms do not have the sensory apparatus to detect threats at a distance, nor do they have a complex behavioral repertoire that can be used for what we are calling behavioral control. That is, adverse events for primitive organisms are generally uncontrollable by their voluntary behavior, and such organisms do not need mechanisms to detect controllability. Thus, the “successfulness” of defensive reflexes is likely related to the duration of the existing threat—if it is prolonged then conservation/withdrawal would be adaptive with energy being shifted to physiological adjustments to threat. It is important to note that 5-HT is phylogenetically very old ( Hen, 1993 ). Moreover, 5-HT has, from the beginning, been involved in controlling and shifting the balance and flow of energy (see Andrews, Bharwani, Lee, Fox, & Thomson, 2015 , for review).

As organisms became more complex, they could detect and identify threats at a distance. And so they developed rich behavioral and cognitive skills that could be used to cope with threats. Control became possible even against threats that persist over time. Clearly, if such control will work this is the best course because it will minimize injury and harm. For complex organisms behavioral control can be possible over threats that are repeated, intermittent, and so persist across time. Thus, conservation/withdrawal and other energy adjustments set in motion by the continuation of threat should be inhibited.

Thus, when encountering a threat we envisage the following scenario. First, defensive behavior will be elicited. The aversive event would activate structures such as the dorsal raphe nucleus. This is a cumulative process with 5-HT building over time, and if the transmitter reaches some threshold in target structures, defensive behaviors become inhibited and energy flow is shifted. However, if control is possible this is detected and leads to the inhibition of this process so that active responding can continue. In addition, plasticity is induced in the prelimbic-to dorsal raphe nucleus circuit so that the system is biased to initially react to aversive events as if they are controllable, thereby prolonging the duration of active responding.

Unresolved Issues

At the level of basic neural circuits, there are several important unresolved issues. The data suggest that there are two important circuits within the ventromedial prefrontal cortex engaged by control that mediate the protective effects of control—a prelimbic-dorsomedial striatum pathway and a prelimbic-dorsal raphe nucleus pathway. The prelimbic-dorsomedial striatum circuit detects control (DETECT) when control is present, and then activates the prelimbic-dorsal raphe nucleus pathway (ACT) to then blunt the behavioral effects of stress. Since Baratta (2015) has shown that the prelimbic neurons that participate in these two circuits are quite discrete, there has to be a pathway from somewhere in the prelimbic-dorsomedial striatum circuit that projects to and activates the prelimbic neurons in the prelimbic- dorsal raphe nucleus pathway, and this pathway is as yet unknown. The “gold standard” discovery of this pathway will require measuring the activity of the prelimbic neurons in each pathway separately , with the critical result being that activity in the prelimbic-dorsomedial striatum pathway precedes activity in the prelimbic- dorsal raphe nucleus pathway. This requires a method that allows the experimenter to know that a prelimbic neuron that is being recorded is in one of these two pathways (most prelimbic neurons are in neither), and which one. This further requires the experimenter to be able to activate or inhibit each pathway selectively . The experiments described earlier in this paper that activated or inhibited prelimbic neurons did so non-selectively, as they involved microinjecting excitatory or inhibitory drugs that would act on all prelimbic neurons.

Thus, the existing neural evidence although strong, it is not conclusive. However genetic/molecular tools are now available that allow these gold standard experiments, and they are underway in the Maier laboratory.

At the psychological level, there are several other loose ends.

As a general statement, neural processes in the prefrontal cortex become narrowed by stress ( Arnsten, 2015 ). Thus, the fact that in an aversive situation the brain seems to detect control as the active ingredient rather than a lack of control, does not mean that the brain cannot detect lack of control in other types of circumstances, such as uncontrollable food or unsolvable cognitive problems, or even loud noise. That is, the findings that we have reviewed do not imply that the brain does not have circuitry to detect non-contingency between events that include actions and outcomes. Rather, it may be that this processing can occur, but is not deployed in situations that are highly aversive such as the original helplessness experiments. So it is important to distinguish between what the brain does under a given set of conditions, and what the brain is capable of under different conditions. This possibility is in need of further research.

Speculations

The neural circuitry explains and predicts phenomena that are not explained or predicted at the psychological level. There are three main takeaways from the neural circuitry that might inform thinking about therapy and psychopathology. The first is that the default response of higher organisms to prolonged bad events seems to be passivity and heightened anxiety and that this is caused by the activation of the dorsal raphe nucleus. The second is that top-down higher cortical processes from the ventromedial prefrontal cortex inhibit this default response. The passivity and heightened anxiety symptoms of learned helplessness map quite well into symptoms of depression ( Seligman 1975 ; Weiss, Simson, Ambrose, Webster, & Hoffman, 1985 ) and perhaps those of posttraumatic stress disorder ( LoLordo & Overmier, 2011 ). The third has to do with the well-established enduring effects of cognitive interventions ( Cuijpers et al., 2013 ). Here we have reviewed research that indicates that the experience of behavioral control over a stressor also has an enduring impact, and have suggested that this occurs because that experience induces plasticity in ventromedial prefrontal cortex neurons that project to midbrain and brainstem stress-responsive structures, leading to their later inhibition. It is tempting to suggest that cognitive therapies operate via the same mechanism. Assuming that learned helplessness models these phenomena, we now speculate on the implications of the neural circuitry particularly for the treatment of depression.

The first blush reaction is that we should measure these structures in humans, and then excite the ventromedial prefrontal cortex and inhibit the dorsal raphe nucleus, pharmacologically, electrically, trans-magnetically or psychologically in therapy. So for example one might ask if the dorsal raphe nucleus is highly excited during deep depression and if it becomes less excited as depression wanes either in time or in therapy. One might ask if medial prefrontal cortical activity inhibits the dorsal raphe nucleus when therapy or medication is successful. One might even look at the effect of medications and of trans-magnetic stimulation of dorsal raphe and medial prefrontal cortical structure during the course of depression. But a set of cautions should temper these speculations. A variety of psychological processes lead to increased ventromedial prefrontal cortex activation as measured by fMRI and also blunt the impact of stressors. However, this does not mean that these processes do so by activating the crucial PL-dorsal raphe nucleus pathway. The ventromedial prefrontal cortex is a large and complex structure encompassing cell types releasing a variety of transmitters and neuropeptides. Moreover, neurons in the ventromedial prefrontal cortex participate in numerous circuits with neurons in other brain regions, and the functions served by these circuits are likely unrelated, except that they share cells in a large piece of heterogeneous geography. The prelimbic neurons that are involved in the prelimbic-dorsomedial striatum and Prelimbic- dorsal raphe nucleus pathways represent an extremely small percentage of the cells in the ventromedial prefrontal cortex and would not contribute measurably to a BOLD signal in the ventromedial prefrontal cortex. Thus, measuring a global ventromedial prefrontal cortex fMRI signal will not remotely imply activation of the control-related critical prelimbic neurons. It might seem that the dorsal raphe nucleus might be usefully imaged, but the dorsal raphe nucleus is a small structure, with roughly 25,000 5-HT cells in the rat and 150,000 in humans. Furthermore, the critical dorsal raphe nucleus5-HT neurons that are involved in mediating the effects of uncontrollable stress and that are inhibited from the prelimbic by control are restricted to the caudal dorsal raphe nucleus ( Grahn et al., 1999 ), maybe 8,000 neurons in the rat and 50,000 in the human. This is too small a number of cells by at least an order of magnitude to be imaged currently.

With regard to therapy, ventromedial prefrontal cortex dysregulation and impaired top-down inhibition of stress responsive limbic and brainstem structures have often been noted (e.g., DeRubeis, Siegle, & Hollon, 2008 ; Hartley & Phelps, 2010 ; Koenigs & Grafman, 2009 ; Rive et al., 2013 ; Shin & Liberzon, 2010 ). There is a growing and complex literature concerning the impact of therapies such as cognitive-behavioral therapy (CBT) on neural function that cannot be reviewed here. However, there are reports that CBT alters ventromedial prefrontal cortex activity and reduces negative emotion relative to wait-listed controls (e.g., Goldin et al., 2013 ).

Reappraisal of situations seen as catastrophic is central to CBT and there is now a large literature that explores the brain regions that might be involved. In reappraisal research subjects make some stimulus or event seem less negative or anxiety arousing (e.g., “imagine that the snake is not poisonous and cannot get at you”). Subjects that are able to successfully reduce negative reactions show reduced amygdala activity and increased activity in lateral and dorsal regions of the prefrontal cortex ( Beauregard, Lévesque, & Bourgouin, 2001 ). Importantly Urry et al. (2006) noted that these regions of the prefrontal cortex do not project to the amygdala, but they do project to the ventromedial prefrontal cortex. She found that when subjects reduced negative emotional reactions successfully, there was a strong negative correlation between amygdala and ventromedial prefrontal cortex activity. This and a variety of other evidence led Ray and Zald (2012) to conclude,

These investigators either implicitly or explicitly describe emotion regulation as the deployment of top-down “cold” cognitive control region of the prefrontal cortex to down regulate bottom-up “hot” reactive processes involving the subcortical limbic regions like the amygdala. Failures in the successful deployment of prefrontal cortex top-down cognitive control mechanisms or overactive bottom-up amygdala processes have been proposed to contribute to several forms of psychopathology (p. 487).

Reappraisal as a tool of therapy is behavioral control. It blunts the impact of a negative event, and likely involves top-down inhibition from the ventro to lower structures. Whether the ventromedial prefrontal cortex activation produced by reappraisal involves the specific pathways that are critical to mediating the impact of behavioral control awaits future research. This encourages speculation that CBT engages the same top-down protective circuitry that has been isolated in the study of behavioral control. After all, CBT teaches cognitive tools that can be used to reduce destructive negative thoughts and emotions. That is, they are taught that there are things that they can do —control.

Why Versus Whither

Given our caution about the multifarious functions and structures of the ventromedial prefrontal cortex, it has not escaped our notice that one such function is prospection, the representation of possible futures ( Seligman et al., 2013 ). In their review of prospection research Gilbert and Wilson (2007) conclude “An extensive body shows that prefeeling depends critically on the ventromedial prefrontal cortex and that people with damage to this area find it difficult to predict the hedonic consequences of future events” (p. 1352).

Notice that the top-down process from the prelimbic to the dorsal raphe nucleus captures the notion of EXPECTing that future bad events will be controllable. This circuit is about the future and it buffers against, but does not annihilate, the default reaction of the dorsal raphe nucleus. A default of helplessness eventually overcome by the experience of mastery over aversive events is compatible with the ontogeny of the human species: beginning life in a state of almost utter helplessness and only gradually learning to control bad events.

The possibility that the prelimbic- dorsal raphe nucleus circuitry involves prospection points to a class of psychological interventions that should be useful and to another class of psychological interventions that should be less useful. This is at the heart of our most speculative thoughts.

The default reaction to past and present bad events may be concurrent passivity and heightened anxiety. These cannot be undone directly or annihilated. They can, however, be inhibited by top-down cortical, control. Treatment can only buffer against past and present events with moves that produce control over bad events in the future : These are therapy's end-runs around bad events. We speculate that it is expectations of a better future that most matter in treatment. Psychotherapy might usefully spend less time on what is likely default and spend more time on what are likely the “end-runs” of DETECTing and then EXPECTing control.

“Why?” is a question that psychotherapy often asks. Perhaps a better question is “whither?” An exhaustive discussion of therapeutic moves that focus on understanding and undoing past and coping with present events as opposed to building buffers for the future is beyond the scope of this paper. So we will only give a few examples. Consider the class of therapy moves in which the patient reviews a past trauma in order to gain insight into its causes or to have catharsis about it. The dorsal raphe nucleus default reaction to trauma suggests that this is an uphill battle that will likely fail. The circuitry suggests that there is not much that can be achieved merely by confronting, understanding and reliving the trauma.

This uphill battle about confronting the past is not the province only of psychodynamic therapy, but it is also common in CBT. Re-appraisal, in general, re-interprets a past or present bad event. All of the following are other examples of a prima facie past focus (see Dobson, 2010 for details): discussion of post-event processing and attendant rumination; discussion of memory biases like selective filtering (where the patient only attended to a negative part of something that happened and ignored the positive parts); behavior chain analysis (where the patient looks at all the steps that led up to a bad outcome, such as an eating or drinking binge, and considers how those steps set him up to ‘fail’); and functional analyses (determining antecedents, behaviors, & consequences).

Similarly many moves in CBT (see Dobson, 2010 for details) focus prima facie on coping with the present. So therapists discuss “mind reading” and “catastrophization,” to facilitate reappraisal of the attributions and meaning a person is making for an ongoing event. Attentional control and mindfulness similarly emphasize the present. Exposure therapies (and emotion-focused therapies) emphasize the present emotional experience and the patient observes how emotion changes over time when he stays in the situation.

We are quick to note, of course, that in the hands of a skilled and experienced therapist these exercises about the past and the present are typically done with the purpose of changing future behavior, such as better recognizing triggers for past maladaptive responses in order to avoid those triggers in the future or gaining insight into catastrophizing in order to learn how to be more optimistic in the future. Nevertheless, from our circuitry speculation, it is the preparation for the future that is likely to be the most effective ingredient and so it is worthwhile to be explicit about the locus of its effectiveness.

Indeed much of cognitive behavioral therapy is actually future–oriented, even if it is not taught in this way. Problem solving, activity scheduling, crisis response plans, role play in assertiveness training, and what doors open when one door closes, all involve simulating future situations and trying to prepare for those effectively. We note that there actually exists a variant, as yet insufficiently validated, of CBT, called “Future Directed Therapy” ( Vilhauer, 2014 ).

Perhaps one CBT “whither” vignette may help the clinician: A young man was distressed about the upcoming one-year anniversary of his psychiatric hospitalization. He was afraid he would be distraught on this anniversary and engage in self-harm.

The therapist could tell that he was anxious and depressed about having been hospitalized, and what this meant for his future. He was probably having some distorted thoughts about it (e.g., “this means I'll always be a fuck-up,” etc.). The therapist considered using classic CBT moves – inquiring about these automatic thoughts and helping him to reappraise them.

Instead, she played dumb: “Wow, the one-year anniversary. How are you going to celebrate it?” He was initially confused. Celebrate? “Well,” she replied, “you've obviously come a really long way since then: You're working again, you're in a great relationship. How would you commemorate that progress, if you wanted to?”

This totally refocused the conversation on future mastery. They also planned ways to prevent self-harm, and they planned the ways that he would capitalize on his progress in the coming year and they explored how he could continue to be in a good place one year from now.

In conclusion, the neural circuitry underlying the phenomenon of learned helplessness strongly suggests that helplessness was not learned in the original experiments. Rather passivity and heightened anxiety are the default mammalian reaction to prolonged bad events. What can be learned is cortical—that bad events will be controllable in the future. The top-down circuitry that descends from the ventromedial prefrontal cortex down to the dorsal raphe nucleus and other structures acts to inhibit this default. We are mindful that in the theory of explanatory style, “hope” consists largely in the habit of expecting that future bad events will not be permanent, global, and uncontrollable, rather they will be temporary, local and controllable ( Seligman, 1991 , pp. 48-49). Such expectations are likely the best natural defense against helplessness and we speculate that the ventromedial prefrontal cortex-dorsal raphe nucleus circuit may be usefully thought of as the “hope circuit.”

Steven Maier, Department of Psychology and Neuroscience, Campus Box 345, University of Colorado at Boulder, Boulder, CO. 80309-0345

Many colleagues and students have contributed to these ideas and experiments over the years, and without them there would be none. Special thanks go to J. Amat, S. Bland, M. Baratta, J. Christianson, A. Der-Avakian, R. Drugan, J. Elstein, R. Grahn, J. Hammack, R.L. Jackson, K. Kubala, S. Maswood, T. Minor, K. Short, P. Sparks, B. Teachman, L.R. Watkins, M. Will, W. Woodmansee, D. Yaden.

Contributor Information

Steven F. Maier, University of Colorado.

Martin E. P. Seligman, University of Pennsylvania.

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Old problem, new tools

One of the psychologists who discovered learned helplessness returns to the topic to pinpoint the phenomenon's neurobiological underpinnings.

By Sadie F. Dingfelder

Monitor Staff

October 2009, Vol 40, No. 9

Print version: page 40

In the 1960s, two University of Pennsylvania psychology graduate students discovered that when dogs received electrical shocks that they could not control, they later showed signs of anxiety and depression, but when dogs could end the shocks by pressing a lever, they didn't. What's more, the dogs that received the uncontrollable shocks in the first experiment didn't even try to escape shocks in a later experiment, even though all they needed to do was jump a low barrier.

The two researchers—Martin E.P. Seligman, PhD, and Steven F. Maier, PhD—termed their discovery "learned helplessness," and their findings are now a staple of introductory psychology textbooks. Seligman went on to further explore the finding, while Maier went in a different direction, retraining as a neuroscientist and studying the effects of stress on the immune system.

But 30 years after the experiment, Maier found himself thinking about that work and wondering if he could find a neural circuit for learned helplessness. With help from students and colleagues at the University of Colorado, where he's a psychology and neuroscience professor, Maier succeeded—and his findings suggest that the dogs from that early experiment were not, in fact, learning helplessness. They were failing to learn control.

"The default position of the brain is to assume that stress is not controllable," he said.

Ancient structures respond

To begin their search for the brain basis of learned helplessness, Maier and his colleagues had to identify a part of the brain that facilitates activation in the amygdala, which plays a major role in fear and anxiety responses, but that inhibits activation in the dorsal periaqueductal gray matter, which triggers fight or flight responses. A review of the literature turned up the dorsal raphe nucleus (DRN) as a likely candidate, since that cluster of neurons in the brain stem releases serotonin into the forebrain and limbic systems as well as the neighboring periaqueductal gray.

To explore the DRN's role in learned helplessness, Maier and his colleagues ran an experiment where they exposed rats to either controllable or uncontrollable tail shocks. The researchers measured the adult rats' DRN serotonin levels throughout the experiment and found that all of the animals' levels spiked when they were first exposed to the shock. But as soon as the rats learned to control the shock by pressing the levers, their serotonin levels dropped.

After the procedure, the researchers placed an unfamiliar juvenile rat in the cage of the rats that had been through the uncontrollable or controllable shock procedures. Usually, adult rats will sniff a juvenile rat, and that's what the animals that experienced controllable shock did, but the rats that had been through the uncontrollable shock procedure cowered in their cages and did not explore the newcomer. Their DRN activation also spiked and stayed high throughout the social stress test, while the other rats' DRNs stayed calm.

"It was the release of serotonin that was responsible for these behavioral effects," concluded Maier.

The mystery, however, was not solved. Past research shows the DRN, which resides in the ancient brain stem, is not smart enough to know whether stress is controllable or not—it just responds to stress in general. Some other part of the brain, said Maier, must be giving the DRN its instructions.

'Cool it, brain stem'

That area, according to research by Maier and his colleagues, appears to be the ventromedial prefrontal cortex (vMPC), a part of the mammalian brain's frontal lobe. In a series of studies published last year, Maier and his colleagues found that when they deactivated the vMPC while animals received controllable shocks, the DRN stayed active, and the rats later showed the signs of anxiety and depression you'd expect only if they had not been in control of the situation. Also, when the researchers activated the vMPC in rats receiving uncontrollable shocks, DRN activation dropped off, and the animals did not show later effects of learned helplessness.

"This is the illusion of control at the level of neurochemistry," Maier said.

Taken together, the findings suggest that in the face of any stressor, the DRN activates the body's ancient stress responses, but if that stressor turns out to be controllable, the vMPC steps in and calms the DRN's response. "It's like the forebrain is saying, 'Cool it, brain stem, we have the situation under control,'" Maier said.

Looking back on his early research, Maier now realizes that the dogs in his seminal study were not learning helplessness, they were just staying in their natural state. Only with training and input from the vMPC, which evolved later than the DRN, do animals learn to relax when a situation is under control.

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Trying to Cure Depression, but Inspiring Torture​

In May, 2002, Martin Seligman, the Director of the Positive Psychology Center, at the University of Pennsylvania, was giving a lecture at the San Diego Naval Base. It had been sponsored by the Joint Personnel Recovery Agency, and some hundred listeners were in attendance. The topic of Seligman’s talk was simple: for a good part of his career, he had studied a concept that came to be known as learned helplessness, the passivity that often comes after we’ve faced problems that we can’t control. That afternoon, he wanted to describe how the data his team had collected over the years could help American personnel—military and civilian alike—“resist torture and evade successful interrogation by their captors,” he recalls. One audience member in particular seemed especially enthused. A year earlier, in December, 2001, he and a colleague had attended a small gathering at Seligman’s house, where 9/11 and anti-terrorism responses had been the topic of conversation. (The colleague had shared his appreciation of Seligman’s work—he was a psychologist himself and Seligman had been an inspiration.) Now, in San Diego, he was taking the opportunity to learn more about the possible direct applications of learned helplessness to the military. Seligman gave it no further thought. Learned helplessness had inspired a lot of people, and many of them, over the years, had expressed their appreciation.

In early December, 2014, the Senate Intelligence Committee released its  report  on the torture techniques used by the Central Intelligence Agency in questioning terror suspects since the 9/11 attacks. The report included hundreds of painfully graphic pages, and it revealed that, starting in 2002, many of the most brutal techniques were developed under the direction of two psychologists contracted by the Agency, James E. Mitchell and Bruce Jessen. Much of the torture was justified through experimental psychology.

“Neither psychologist had any experience as an interrogator, nor did either have specialized knowledge of al-Qa’ida, a background in counterterrorism, or any relevant cultural or linguistic expertise,” the report stated. But all the same, they had created what they thought would be a winning approach, “theories of interrogation based on ‘learned helplessness,’ ” which, the report specified, was “the theory that detainees might become passive and depressed in response to adverse or uncontrollable events, and would thus cooperate and provide information.” One of the psychologists—the one who went by the pseudonym Grayson Swigert, who has been  identified as Mitchell , “had reviewed research on ‘learned helplessness,’ ” and had “theorized that inducing such a state could encourage a detainee to cooperate and provide information.” He had also, months before he began to advise the C.I.A., attended Seligman’s post-9/11 gathering. He had been the one to come up to speak with the psychologist and to express his admiration.

To understand the nature of learned helplessness, one needs to travel back to Seligman’s early graduate-school days in the laboratory of Richard Solomon at the University of Pennsylvania. When Seligman began his studies, Solomon’s lab was working with dogs on a phenomenon that  Ivan Pavlov  had first identified as aversive conditioning or avoidance learning. The  researchers  administered shocks to the animals, accompanied by tones or lights, so that they would come to associate the tone or light stimuli with the shock’s onset, and, in some cases, then learn to avoid the shock by jumping over a barrier. Solomon would then  work  to see if he could get the dogs to, in effect, unlearn the association. When Seligman arrived at the lab, he noticed that some of the dogs had started to act rather strangely. Instead of trying to figure out how to avoid a new shock, they just sat there. They didn’t even try to figure it out. Teaming up with fellow graduate student Steven Maier, Seligman began to study what was going on.

In a  series of experiments , Seligman and Maier first attached dogs to a harness, a kind of rubberized cloth hammock, with holes for the dogs’ legs to dangle free. As the dogs hung, their heads were kept in place by two panels, which they could easily press with their heads. At random intervals, coming between sixty and ninety seconds apart, they would receive a series of shocks to their hind feet. Some of the dogs could control the shocks with a simple press of the head against either of the panels; for others, the head-pressing did nothing. The moment the dogs with the functional panels touched either one, the shock ended. Otherwise, it lasted for thirty seconds to begin with, and for increasingly shorter durations thereafter.

The next day, each dog was set free inside a shuttle box, a two-compartment cage separated by an adjustable barrier. Each time the lights in the box went off, half of the floor would become electrified, shocking the poor animals. But if the dog jumped over the barrier and into the next cage, the shock could be avoided. This time, each dog had the power to end its discomfort quite easily.

When Seligman and Maier analyzed the results, they found a consistent pattern. The dogs that had learned to avoid the shocks by pressing their heads against the panels on the first day were quick to jump the barrier on day two. Not a single dog failed to learn to jump quickly after the first go-around. Those that had been unable to escape the shocks, though, weren’t even trying. They were free to move, explore, and escape—but they didn’t. Two-thirds of them were still hovering in the electrified side of the box by the end of the experiment—and for the remaining third, the average number of trials to learn to escape was just more than seven, out of the total ten. A week later, five of the six dogs that had failed to learn were still unwilling to even try: they once again failed the shuttle-box test. The effect of the harness experiment was been both severe and lasting.

Seligman and Maier called what they were observing “learned helplessness”—the same term that would resurface in Seligman’s lecture and in the Senate torture report. The phenomenon was reliably strong, reliably broad (that is, transferred from one situation to another), and reliably difficult to change once it set in. It was motivational (you no longer even try), emotional (you whimper and grow resigned), and cognitive (you generalize one experience to apply to a broader existence). And it wasn’t confined to dogs. Soon, others picked up on their work, demonstrating similar effects in  cats ,  fish , rats, and the favorite of all experimental animals,  college students.

But Seligman didn’t stop his research there. He had told his supervisor that he didn’t believe in causing suffering unless it had some inherent value that would lead to bettering lives, both canine and human. So he and Maier set out to figure out a way to reverse the effect of learned helplessness in the dogs. What they found was that one simple tweak could stop the passivity from developing. When the researchers first put all the dogs in the shuttle box, where the shock was controllable by a jump, and, only then, into the inescapable harness, the effect of the harness was broken: now, even though the dogs were being bombarded by shocks, they didn’t give up. They kept trying to control the situation, pressing the panels despite the lack of feedback. And when they were again put into the box, they didn’t cower. Instead, they immediately reclaimed their ability to avoid shocks.

That was what Seligman had been after. If dogs could be inured to learned helplessness, then, potentially, so could people.

So what had the dogs actually learned—and how could that lesson be translated to human beings? Seligman inferred that the canines that went on to escape shocks had realized something important—not all shocks are equal, and it doesn’t hurt to keep trying to get away. Those that didn’t likely went through a different reasoning process: Nothing I do here helps, so why even bother trying?

In 1978,  working with  his graduate student, Lyn Abramson, and John Teasdale, a psychologist at Oxford specializing in depression, Seligman began to apply the model to humans. Humans, the group posited, differed from other animals in one significant respect: when they find themselves helpless, they explicitly ask  why  that is the case. The answer, in turn, can differ along three different lines: whether the electric shock, so to speak, is seen as permanent or transient, pervasive or limited, and personal or incidental. Seligman called these differences our explanatory style. Some people were naturally inclined to believe that bad things will keep happening to us and that they are our fault. Some were naturally inclined toward the opposite—bad things are happening now, but they’ll stop and they’re not our fault. The former were those who were prone to depression; the latter were those who tended to bounce back. Seligman believed that humans, like dogs, could be taught to become more resilient, a phenomenon he called learned optimism.

For the next twenty years, Seligman worked with Aaron Beck, the psychiatrist who came up with the therapeutic approach of Cognitive Behavioral Therapy, or C.B.T., one of the most consistently successful methods of helping people overcome depression, to integrate his findings on learned helplessness into actual behavioral therapies. In 1984, he  published  a review of the evidence. First, he and his colleagues had found that the way people explained bad events to themselves really did link closely to depression risk. It was true in students, in people from low socioeconomic backgrounds, in children, and, predictably, in depressed patients. And, importantly, training people to change their explanatory habits—to more narrow, external, and transient—seemed to help them overcome existing depression and, in some cases, prevent its onset even when other risk factors were high.

In 1995 , Seligman and his colleagues published the results of a longitudinal study of depression, or, rather, its prevention, in schoolchildren. He and his colleagues had recruited fifth- and sixth-graders from two school districts in a Philadelphia suburb, to participate in what they called a prevention program. Over the course of three months, children who either expressed symptoms of depression already or had tested at high risk for their development met for an hour and a half each week in groups of ten to twelve. At each meeting, a psychology graduate student took them through the steps of two types of therapy centered around explanatory style, one aimed at cognition— how they thought about things—and one at social problem-solving.

The cognitive program taught the kids to identify when they were having negative thoughts, to evaluate those thoughts objectively, and then to come up with alternatives. It also had them reframe any pessimistic explanations that they found themselves giving—my mom is sad, because I did something wrong—for more optimistic and realistic ones—my mom is sad, because she had a long day at work. Two weeks prior to the start of the program, one week after its end, and every six months after that, the researchers gave each child an array of tests to gauge her level of depression.

Not only were the children enrolled in the prevention program less depressed than those in the control group—it consisted of children from a neighboring district who were matched on all criteria and risk factors—but, over time, the difference grew more pronounced. After one year, twenty-nine per cent of the children in the control group reported mild to severe depression, compared to 7.4 per cent of those who had enrolled in the prevention program. At the end of the two years, forty-four per cent of the children in the control group had developed a form of depression. Only twenty-two per cent of the treatment group had done so. The improvements hinged largely on changes in the children’s explanatory style: the ones in the prevention group had learned how to create explanations that rendered them hopeful instead of hopeless.

Since then, the findings have been expanded to a major longitudinal project, the  Penn Resiliency Program . The program to date has included more than seventeen controlled studies and has measured the approach in more than twenty-five hundred children and adolescents. Its current projects include an ongoing one in two Philadelphia school districts; a sister program in South Tyneside, Hertfordshire, and Manchester, in England; an offshoot in Australia’s Geelong Grammar School; and a program specifically targeted at early adolescent girls, the Girls in Transition Program. In 2009, a  meta-analysis  of the data found that students who had participated in versions of the cognitive-training program showed fewer depressive symptoms than non-participants in assessments performed six to eight months after and a year after the program’s conclusion.

This work, according to Seligman, who, in 1998, became president of the American Psychological Association, is his legacy. “I have spent my life trying to cure learned helplessness,” he told me.

But then came the torture report. And when he heard what his research had been used to justify, he was both shocked and mystified. He told me that he was “grieved that good science, which has helped many people overcome depression, may have been used for such a bad purpose as torture.” Not only that, but its very use, he felt, was contrary to the core of his findings. He is no scholar of interrogation, he says, but as he understands it, “the point of interrogation is to get at the truth and to have the person believe that telling the truth will lead to good treatment.” Does learned helplessness actually achieve that end?

Here’s what we know: learned helplessness can indeed be a severe form of torture. The inability to control one’s environment has repeatedly been shown to create not only anger and frustration but, eventually, deep and often insurmountable depression. In a sense, inducing learned helplessness makes a person give up. We shouldn’t forget the high price at which the learned-helplessness findings came: many of the animals used in the studies died or became severely ill shortly thereafter. So is learned helplessness an effective way of causing incredible pain? No doubt.

But here’s the more relevant question: Does the condition, in turn, make someone more likely to tell the truth and give up important information that had previously remained hidden? Here we have no direct data—after all, there have never been controlled torture trials that we know of—but we do have some theoretical basis in the study of severe depression to suggest that it will do no such thing. People who’ve given up lack all incentive. Once they are in that state of hopelessness , there is no longer a way to motivate them. Absent any possible inducement or motivation, most people just want to quit. The threat of pain or even death no longer makes much of a difference: Nothing I do or say matters, so why bother? A person in a state of learned helplessness is someone who is passive, someone who has abandoned all active will and desire. He can tell the truth, yes, but why? Lying or saying whatever it is that the torturer wants to hear is just as likely to attain the same result. A person without motivation is not a person who can be induced to tell deep truths: the incentive simply isn’t there.

“I think learned helplessness would make someone less defiant and more likely to compliantly tell the interrogator what he wants to hear,” Seligman said. “It would also likely undermine the belief that telling the truth will lead to good treatment.” In other words, it would do the opposite of what its users in this particular context intended.

Seligman says that he isn’t the father of learned helplessness. He’s the father of positive psychology: the study of how to go about identifying and nurturing positive emotion, and using it to withstand the negative. Learned helplessness, at the end, isn’t about helplessness at all—it’s about empowerment and control.