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Journal of Pharmacology and Experimental Therapeutics

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Oxidative Stress and the Central Nervous System

Biochemical integrity of the brain is vital for normal functioning of the central nervous system (CNS). One of the factors contributing to cerebral biochemical impairment is a chemical process called oxidative stress. Oxidative stress occurs upon excessive free radical production resulting from an insufficiency of the counteracting antioxidant response system. The brain, with its high oxygen consumption and lipid-rich content, is highly susceptible to oxidative stress. Therefore, oxidative stress–induced damage to the brain has a strong potential to negatively impact normal CNS functions. Although oxidative stress has historically been considered to be involved mainly in neurodegenerative disorders such as Alzheimer disease, Huntington disease, and Parkinson disease, its involvement in neuropsychiatric disorders, including anxiety disorders and depression, is beginning to be recognized. This review is a discussion of the relevance of cerebral oxidative stress to impairment of emotional and mental well-being.

Introduction

Oxidative phosphorylation occurring in the mitochondria is a major source of ATP. As a by-product, this process produces free radicals or reactive oxygen species (ROS), reactive nitrogen species (RNS), and carbon- and sulfur-centered radicals ( Pero et al., 1990 ). In moderate or low amounts ROS are considered essential for neuronal development and function, whereas excessive levels are hazardous. ROS-generated nitrous oxide and carbon monoxide promote important physiologic functions, such as long-term potentiation (LTP) via glutamate-dependent mechanisms ( O’Dell et al., 1991 ; Stevens and Wang, 1993 ; Verma et al., 1993 ; Zhuo et al., 1993 ; Knapp and Klann, 2002 ). Under normal conditions, deleterious effects of ROS production during aerobic metabolism are neutralized by the antioxidant system and in this manner the brain effectively regulates its oxygen consumption and redox generation capacity. When ROS production exceeds scavenging capacity of antioxidant response system, extensive protein oxidation and lipid peroxidation occurs, causing oxidative damage, cellular degeneration, and even functional decline. For example, high ROS concentrations reportedly diminish LTP and synaptic signaling and brain plasticity mechanisms ( O’Dell et al., 1991 ; Stevens and Wang, 1993 ; Verma et al., 1993 ; Zhuo et al., 1993 ; Knapp and Klann, 2002 ). This is regarded as a state of oxidative stress and becomes particularly hazardous for normal functioning of the brain.

Oxidative stress is often described as a self-propagating phenomenon on the basis of observations that when oxidative stress–induced excessive ROS release triggers cellular damage, damaged macromolecules themselves may behave as and/or become ROS. Consequently, the brain, with its rich lipid content, high energy demand, and weak antioxidant capacity becomes an easy target of excessive oxidative insult ( Hulbert et al., 2007 ). Phospholipids in the brain are particularly vulnerable entities for ROS-mediated peroxidation, but proteins and DNA also are targeted by ROS, which becomes particularly problematic during aging, as aged brains have been reported to exhibit high levels of oxidative stress–induced mutations in the mitochondrial DNA ( Gross et al., 1969 ; Chomyn and Attardi, 2003 ; Kraytsberg et al., 2003 ; Trifunovic et al., 2004 ). Therefore, ROS accumulation is a cellular threat that, if it exceeds or bypasses counteracting mechanisms, can cause significant neuronal damage.

Two kinds of protective mechanisms operate in the brain to tackle the threat posed by ROS, the antioxidant enzyme system and the low-molecular-weight antioxidants ( Kohen et al., 1999 , 2000 ). The antioxidant enzyme system includes superoxide dismutase (SOD), glyoxalase, glutathione reductase, glutathione peroxidase, and catalase (CAT) ( Griendling et al., 2000 ). SOD enzymes, including Cu-Zn SOD and Mn-SOD, facilitate spontaneous dismutation of superoxide radicals to generate H 2 O 2 , which is further removed by CAT and glutathione peroxidase enzymes ( Saso and Firuzi, 2014 ). The low-molecular-weight antioxidants include glutathione, uric acid, ascorbic acid, and melatonin, which offer neutralizing functions by causing chelation of transition metals ( Chance et al., 1979 ). Glutathione, which occurs in reduced (GSH) and also in oxidized form (glutathione disulfide) is the most important nonenzymatic endogenous antioxidant and can be regenerated by glutathione reductase with the consumption of NADPH ( Gul et al., 2000 ). In this manner optimum levels of reduced GSH are maintained ( Kohen and Nyska, 2002 ; Halliwell, 2006 ). The endogenous ratio of GSH to glutathione disulfide is considered an indicator of redox homeostasis within a cell. Higher levels of GSH also serve as a cofactor for other enzymes including glyoxalase and peroxidase ( Kohen and Nyska, 2002 ).

In response to oxidative and nitrosative stress, cells increase their antioxidant defenses through activation of nuclear factor erythroid 2–related factor (Nrf2), an important transcription factor ( Maes et al., 2011 ). Nrf2 is a key component of this control system and recognizes the antioxidant response element (ARE) found in the promoter regions of many genes that encode antioxidants and detoxification enzymes such as heme oxygenase 1 (HO-1), NAD(P)H dehydrogenase quinone 1, SOD1, glutathione peroxidase 1 (GPx1), and CAT ( Itoh et al., 1997 ). Thus, Nrf2 pathway activation occurs to combat the accumulation of ROS and RNS species. Owing to its protective properties, Nrf2 has been proposed as a pharmacological target in pathologies with neuroinflammatory and oxidative features, including neurodegenerative and neuropsychiatric diseases. When activated, Nrf2 increases the expression of several endogenous antioxidants. And, upon persistent inflammation and increased ROS levels, as observed during several psychiatric episodes, tissue antioxidant defense mechanisms are saturated to the point they become ineffective ( Anderson and Maes, 2014 ). Cytosolic enzymes such as glyoxalase I by detoxifying methylglyoxal offer protection from oxidative damage ( Distler and Palmer, 2012 ). methylglyoxal generates highly oxidative advanced glycation end products and can further induce oxidative stress and cause cell death ( Uribarri et al., 2010 ).

It is clear that ROS play a crucial pathophysiological role ( Campese et al., 2004 ) and that ROS accumulation increases the susceptibility of brain tissue to damage. Mechanisms by which ROS cause cerebral tissue damage are not well understood but ROS are reported to trigger a variety of molecular cascades that increase blood-brain barrier permeability and alter brain morphology, thus causing neuroinflammation, and neuronal death ( Gu et al., 2011 ). Involvement of hypothalamic-pituitary-adrenal axis–mediated glucocorticoid receptor signaling, glutamate toxicity, and N -methyl- d -aspartate receptor signaling systems also has been suggested ( Makino et al., 1996 ; Okamoto et al., 1999 ; Tanaka et al., 1999 ; Albrecht et al., 2010 ; Nguyen et al., 2011 ). Thus, evidence of increased brain oxidative damage in the development of central nervous system pathologies has been reported for neurodegenerative diseases, including Alzheimer disease, Parkinson disease, and amyotrophic lateral sclerosis, cerebrovascular disorders, demyelinating diseases, and psychiatric disorders ( Sorce and Krause, 2009 ).

Oxidative Stress and Neurodegenerative Disorders

Neurodegenerative disorders commonly associated with muscular, dementic, and cognitive deficits exhibit brain atrophy, neurofibrillary tangles, plaques, and aggregates as pathologic hallmarks of the disease ( Kipps et al., 2005 ; Obeso et al., 2008 ; Gandhi and Abramov, 2012 ). Alzheimer disease, Parkinson disease (PD), and Huntington disease are commonly occurring neurodegenerative disorders that involve neurotoxic aggregation of specific proteins in the brain. Accumulation of misfolded tau and amyloid β proteins occurs in Alzheimer disease, and α -synuclein and mutant Huntington protein (mHtt) accumulate in PD and Huntington disease, respectively. Cause and effect relationship between oxidative stress and these protein aggregates has been theorized. Some studies have reported age-associated increase in oxidative stress–led ROS as a contributor to formation of neuronal plaque, α- synuclein, and mHtt ( Li et al., 2013 ), and other studies have suggested a role for amyloid β protein formation in ROS production ( Behl et al., 1997 ; Abramov and Duchen, 2005 ; Shelat et al., 2008 ). Likewise with regard to PD pathology, it is reported that oxidative stress promotes α -synuclein aggregation in dopaminergic neurons, and that α -synuclein further generates intracellular ROS ( Xiang et al., 2013 ). Furthermore, neuronal cell culture studies have implicated free radicals in misfolding and accumulation of mHtt-induced neurotoxicity in PC12 cells. Whereas accumulation of mHtt led to decrease in antioxidant protein peroxiredoxin Prx1, the overexpressed wild-type Prx1 significantly reduced mHtt-induced toxicity ( Pitts et al., 2012 ). Amyloid β -mediated ROS production was reported to induce lipid peroxidation, causing impaired membrane permeability and activating excitotoxicity mechanisms because of increased calcium (Ca 2+ ) influx. This is believed to significantly alter neurotransmission and cognitive functions. In fact, several studies have implicated ROS in amyloid β -induced impairment in LTP, a cellular correlate of learning and memory ( Dumont et al., 2009 ; Ma et al., 2011 ; Ma and Klann, 2012 ; Parajuli et al., 2013 ), also a consequence of aberrant neuronal transmission.

Oxidative Stress and Neuropsychiatric Disorders

Neuropsychiatric disorders are complex and heterogeneous disorders that not only negatively impact quality of life but also significantly affect behavior and cognitive functions ( Post, 1992 ; Kessler, 1997 ). Several pathophysiological mechanisms have been implicated in these orders, including genetic predisposition, monoamine deficiency, circadian disruptions, hypercortisolemia, and inflammation ( Belmaker and Agam, 2008 ). The involvement of oxidative stress mechanisms have also been suggested in some psychiatric illnesses, including depression, anxiety disorders, schizophrenia, and autism spectrum disorders ( Valko et al., 2007 ; Ng et al., 2008 ; Bouayed et al., 2009 ). Increased levels of ROS and RNS ( Suzuki and Colasanti, 2001 ; Dhir and Kulkarni, 2011 ; Maes et al., 2011 ) and altered levels of antioxidant glutathione (GSH) were reported in postmortem brain samples of depressed individuals ( Gawryluk et al., 2011 ). Actually, oxidative stress mechanisms have been suggested as targets for novel antidepressants ( Lee et al., 2013 ). This seems reasonable considering reported occurrence of inflammation, oxidative and nitrosative stress, as well as declining levels of plasma concentrations and activity of several key antioxidants in samples from depressed subjects ( Maes et al., 2011 ).

An association between depression and polymorphisms in SOD and CAT genes is also known ( Maes et al., 2011 ). The hypothesis is that the antidepressants exert their therapeutic effect by suppressing proinflammatory cytokines and ROS/RNS production or by enhancing antioxidant defense ( Behr et al., 2012 ). There seems to be strong data to support that depression is accompanied with oxidative stress and that, perhaps, augmentation of antioxidant defenses is one of the mechanisms underlying the neuroprotective effects of antidepressants ( Wu et al., 2013 ). Oxidative stress mechanisms also have been tied to schizophrenia and bipolar disorder. Increased levels of plasma SOD activities were reported in chronic schizophrenic patients who were put on antipsychotic medication, and SOD activities were negatively correlated with positive symptoms of schizophrenics ( Ranjekar et al., 2003 ). Levels of other antioxidants, including glutathione peroxidase (GSH-Px), also have been implicated ( Abdalla et al., 1986 ; Stoklasová et al., 1986 ; Buckman et al., 1987 ; Altuntas et al., 2000 ). It has been suggested that low GSH-Px is a contributing factor to structural brain abnormalities ( Buckman et al., 1990 ; Yao and Reddy, 2011 ). Several studies have reported that patients with bipolar disorder have significant alterations in antioxidant enzymes, lipid peroxidation, and nitric oxide levels ( Andreazza et al., 2008 ), suggesting the role of free radicals and antioxidants in the pathophysiology of bipolar disorder ( Berk et al., 2011 ; Magalhães et al., 2011 ; Sarris et al., 2011 ). Accumulating evidence implicates free radical–mediated pathology, altered antioxidant capacity, neurotoxicity, and inflammation in neuropsychiatric and neurodegenerative disorders.

Oxidative Stress and the Brain

The precise chain of events occurring within the central nervous system that potentially causes or leads to oxidative stress–induced behavioral and cognitive decline is an interesting topic and can be examined at multiple levels. Biochemically, it is evident that different neurons have different levels of vulnerability to oxidative stress. For example, hippocampus, amygdala, and cerebellar granule cells have been reported as the most susceptible to oxidative stress in some studies ( Wang and Michaelis, 2010 ), and consequently are purported to be the first to undergo functional decline. Our own preclinical work has suggested that behavioral and cognitive deficits are attributed to three brain regions: hippocampus, amygdala, and prefrontal cortex (PFC) ( Masood et al., 2008 ; Salim et al., 2010a , b , 2011a , b ; Patki et al., 2013a ; 2013b ; Solanki et al., 2015 ). Hippocampus seems to be at the hot seat, and it appears that this brain region undergoes major biochemical changes that ultimately determine neuronal connections and function. Within the hippocampus, it is well known that the dentate gyrus–cornu ammonis (CA)3 system exhibits structural plasticity with regenerative/remodeling capacity ( Popov and Bocharova, 1992 ; Sousa et al., 2000 ; McEwen, 2008 ). Furthermore, several studies have suggested that pyramidal cells of CA3 and granule cells of the dentate gyrus (DG) are oxidative stress–prone areas, whereas others have suggested that pyramidal cells of CA1 are more susceptible to oxidative damage ( Bearden et al., 2009 ; Cruz-Sánchez et al., 2010 ; Chang et al., 2012 ; Huang et al., 2012 , 2013 ; Uysal et al., 2012 ). Regardless, region-specific elevation of oxidative stress within cornu ammonis areas CA1 and CA3, and DG is important and can have significant functional consequences. This is particularly significant as the DG has a preferential role in learning and memory function, and ventral hippocampus is implicated in anxiety and depression.

Furthermore, amygdala and PFC might undergo dendritic alterations, as evidenced in situations of chronic stress. Dendritic shrinking in medial PFC and dendritic growth in amygdalar neurons in response to stress also has been reported ( Wellman, 2001 ; Vyas et al., 2002 ; Kreibich and Blendy 2004 ; Brown et al., 2005 ; Radley et al., 2006 ). Stressful stimuli are known to alter prefrontal dendritic architecture and neuronal connectivity within the PFC ( Liston et al., 2009 ; Luethi et al., 2009 ). Interestingly, higher vulnerability of the hippocampus and amygdala to oxidative stress and breakdown of antioxidant defense system is evident. Therefore, it seems highly plausible that oxidative stress in the brain compromises biochemical integrity of the hippocampus and the amygdala. It is well known that the hippocampal DG-CA3 system regulates structural plasticity, regenerative/remodeling capacity, as well as neurogenesis factors like brain-derived neurotrophic factor ( Wang and Michaelis, 2010 ). It has also been suggested that the pyramidal cells of CA1 and CA3 and granule cells of DG are highly susceptible to oxidative damage. Thus, oxidative damage of DG-CA function may diminish cell proliferation, impair remodeling capacity, alter structural plasticity, and disrupt neurogenesis, collectively disturbing normal synaptic neurotransmission. And, oxidative stress–initiated neuroendocrine alterations within the amygdala, including amygdalar hyperactivity and dendritic shrinking ( Wellman, 2001 ; Vyas et al., 2002 ; Kreibich and Blendy 2004 ; Brown et al., 2005 ; Radley et al., 2006 ; Wood et al., 2010 ), can further potentiate synaptic disturbances by disrupting the hippocampus-amygdala projections. Furthermore, free radicals are known to oxidize the extracellular sites of glutamatergic N -methyl- d -aspartate receptors, leading to attenuation of LTP and synaptic neurotransmission ( Haxaire et al., 2012 ; Lee et al., 2012 ; Rai et al., 2013 ). Collectively, these events offer an attractive explanation for oxidative stress–induced behavioral and cognitive impairment.

Perhaps, psychologic stress disrupts oxidant-antioxidant balance within the brain, causing impairment of antioxidant enzyme function. This leads to glutathione depletion and increases oxidative stress. Simultaneously occurring glutamate toxicity, calcium imbalance, and mitochondrial impairment collectively intensify oxidative stress, causing biochemical distress in the brain. This disrupts neurocircuitry and weakens hippocampal, amygdalar, and cortical connections, ultimately causing behavioral and cognitive deficits ( Fig. 1 ). It seems reasonable to suggest that, perhaps, tight regulation of oxidative stress, either by enhancing the activity of enzymes of antioxidant defense or by directly quenching pro-oxidants, offers the potential to limit psychiatric symptoms. Thus, data discussed in this review provides a basis for a biologically plausible oxidative stress hypothesis that would explain how oxidative damage might cause psychiatric symptoms.

Schematic representation of how oxidative stress might lead to cognitive and behavioral deficits. Persistent psychologic stress disrupts oxidant-antioxidant balance within the brain, causing reduction in antioxidant enzyme function of glyoxalase (GLO)-1, glutathione reductase (GSR)-1, manganese superoxide dismutase (Mn SOD), and Cu/Zn SOD. This leads to glutathione depletion, causing oxidative stress. Simultaneously occurring glutamate toxicity, calcium imbalance, and mitochondrial impairment collectively intensify oxidative stress, causing biochemical distress in the brain. This disrupts neurocircuitry, weakening hippocampal, amygdalar, and cortical connections and ultimately causing behavioral and cognitive deficits.

Acknowledgments

The author’s former and present graduate students, Naimesh Solanki, Ankita Salvi, Hesong Lui, and Fatin Atrooz, are gratefully acknowledged for their hard work in this area of research. Undergraduate students Nada Sarraj, Farida Allam, Amber Ansari, Faizan Jafri, Eisha Khan, Phoebe Dantoin, and Safiyya Zaidi were very helpful in conducting animal behavior work.

Abbreviations

Authorship Contributions

Wrote or contributed to the writing of the manuscript: Salim.

Funding for this research was provided by a grant from the National Institutes of Health ( 2R15 MH093918-02 ) awarded to S.S.

dx.doi.org/10.1124/jpet.116.237503 .

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• Histamine H3-receptor-induced attenuation of norepinephrine exocytosis: a decreased protein kinase a activity mediates a reduction in intracellular calcium. .  312. 2004
• Nitric oxide (NO)-releasing naproxen (HCT-3012 [(S)-6-methoxy-alpha-methyl-2-naphthaleneacetic Acid 4-(nitrooxy)butyl ester]) interactions with aspirin in gastric mucosa of arthritic rats reveal a role for aspirin-triggered lipoxin, prostaglandins, and NO in gastric protection. .  311. 2004
• Disruption of the Ah receptor gene alters the susceptibility of mice to oxygen-mediated regulation of pulmonary and hepatic cytochromes P4501A expression and exacerbates hyperoxic lung injury. .  310. 2004
• 2-furoyl-LIGRLO-amide: a potent and selective proteinase-activated receptor 2 agonist. .  309. 2004
• Cooperation between aspirin-triggered lipoxin and nitric oxide (NO) mediates antiadhesive properties of 2-(Acetyloxy)benzoic acid 3-(nitrooxymethyl)phenyl ester (NCX-4016) (NO-aspirin) on neutrophil-endothelial cell adherence. .  309. 2004
• Histamine H1 and H2 receptor gene and protein levels are differentially expressed in the hearts of rodents and humans. .  309. 2004
• Simultaneous modeling of abciximab plasma concentrations and ex vivo pharmacodynamics in patients undergoing coronary angioplasty. .  307. 2003
• Suppressed prolactin response to dynorphin A1-13 in methadone-maintained versus control subjects. .  306. 2003
• Ectonucleotidase in sympathetic nerve endings modulates ATP and norepinephrine exocytosis in myocardial ischemia. .  306. 2003
• Selective depression by general anesthetics of glutamate versus GABA release from isolated cortical nerve terminals. .  304. 2003
• Proteinase-activated receptor-2 (PAR2): vascular effects of a PAR2-derived activating peptide via a receptor different than PAR2. .  303. 2002
• Ischemia promotes renin activation and angiotensin formation in sympathetic nerve terminals isolated from the human heart: contribution to carrier-mediated norepinephrine release. .  302. 2002
• EctoNucleotidase in cardiac sympathetic nerve endings modulates ATP-mediated feedback of norepinephrine release. .  300. 2002
• Regulation of cyclooxygenase by the heme-heme oxygenase system in microvessel endothelial cells. .  300. 2002
• State-dependent block of rabbit vascular smooth muscle delayed rectifier and Kv1.5 channels by inhibitors of cytochrome P450-dependent enzymes. .  298. 2001
• Anticonvulsant and adverse effects of avermectin analogs in mice are mediated through the gamma-aminobutyric acid(A) receptor. .  295. 2000
• Opioid receptor imaging with positron emission tomography and [(18)F]cyclofoxy in long-term, methadone-treated former heroin addicts. .  295. 2000
• Angiotensin-converting enzyme-independent angiotensin formation in a human model of myocardial ischemia: modulation of norepinephrine release by angiotensin type 1 and angiotensin type 2 receptors. .  294. 2000
• Cannabinoids protect cells from oxidative cell death: a receptor-independent mechanism. .  293. 2000
• Adenoviral vector-mediated transfer of human heme oxygenase in rats decreases renal heme-dependent arachidonic acid epoxygenase activity. .  293. 2000
• LLC-PK(1) cells stably expressing the human norepinephrine transporter: A functional model of carrier-mediated norepinephrine release in protracted myocardial ischemia. .  291. 1999
• Differential effects of heme oxygenase isoforms on heme mediation of endothelial intracellular adhesion molecule 1 expression. .  291. 1999
• Bradykinin activates a cross-signaling pathway between sensory and adrenergic nerve endings in the heart: a novel mechanism of ischemic norepinephrine release? .  290. 1999
• Bradykinin promotes ischemic norepinephrine release in guinea pig and human hearts. .  288. 1999
• Large receptor reserve for cannabinoid actions in the central nervous system. .  288. 1999
• Dynorphin A1-13 causes elevation of serum levels of prolactin through an opioid receptor mechanism in humans: gender differences and implications for modulation of dopaminergic tone in the treatment of addictions. .  288. 1999
• Pharmacokinetics of IgG and IgM anti-ganglioside antibodies in rats and monkeys after intrathecal administration. .  284. 1998
• The competitive alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate receptor antagonist LY293558 attenuates and reverses analgesic tolerance to morphine but not to delta or kappa opioids. .  283. 1997
• Activation of histamine H3 receptors inhibits carrier-mediated norepinephrine release in a human model of protracted myocardial ischemia. .  283. 1997
• d-Methadone is antinociceptive in the rat formalin test. .  283. 1997
• Therapeutic trial of reconstituted human high-density lipoprotein in a canine model of gram-negative septic shock. .  272. 1995
• Unmasking of activated histamine H3-receptors in myocardial ischemia: their role as regulators of exocytotic norepinephrine release. .  271. 1994
• Histamine H3-receptor signaling in the heart: possible involvement of Gi/Go proteins and N-type Ca++ channels. .  269. 1994
• Modulation of morphine tolerance by the competitive N-methyl-D-aspartate receptor antagonist LY274614: assessment of opioid receptor changes. .  268. 1994
• Nifedipine inhibits the induction of nitric oxide synthase by bacterial lipopolysaccharide. .  265. 1993
• Attenuation and reversal of morphine tolerance by the competitive N-methyl-D-aspartate receptor antagonist, LY274614. .  264. 1993
• A central nervous system action of nitric oxide in blood pressure regulation. .  262. 1992
• Activation of protein kinase A is necessary but not sufficient for ethanol-induced desensitization of cyclic AMP production. .  262. 1992
• Mechanism of vascular smooth muscle contraction by sodium fluoride in the isolated aorta of rat and rabbit. .  258. 1991
• Tin(Sn+4)-diiododeuteroporphyrin; an in vitro and in vivo inhibitor of heme oxygenase with substantially reduced photoactive properties. .  257. 1991
• The hemodynamic effects of S-nitrosocaptopril in anesthetized dogs. .  256. 1991
• L-arginine, but not N alpha-benzoyl-L-arginine ethyl ester, is a precursor of endothelium-derived relaxing factor. .  255. 1990
• Electrophysiologic effects of ethanol in human brain xenografts in oculo: antagonism by Ro15-4513. .  254. 1990
• Comparative behavioral, neurochemical and pharmacological activities of dihydropyridine calcium channel activating drugs. .  253. 1990
• Cardiac dysfunction caused by recombinant human C5A anaphylatoxin: mediation by histamine, adenosine and cyclooxygenase arachidonate metabolites. .  253. 1990
• Comparison between the vasoactive actions of endothelin and arginine vasopressin in pithed rats after pretreatment with BAY K 8644, nifedipine or pertussis toxin. .  253. 1990
• Pharmacological characterization of morphine-6 beta-glucuronide, a very potent morphine metabolite. .  251. 1989
• S-nitrosocaptopril. I. Molecular characterization and effects on the vasculature and on platelets. .  249. 1989
• S-nitrosocaptopril. II. Effects on vascular reactivity. .  249. 1989
• Morphine-induced tachycardia in fetal lambs: a bell-shaped dose-response curve. .  249. 1989
• C3a-induced contraction of guinea pig ileum consists of two components: fast histamine-mediated and slow prostanoid-mediated. .  248. 1989
• Adenosine promotes histamine H1-mediated negative chronotropic and inotropic effects on human atrial myocardium. .  247. 1988
• Positive inotropic effect of histamine on guinea pig left atrium: H1-receptor-induced stimulation of phosphoinositide turnover. .  247. 1988
• Activation of the third complement component (C3) and C3a generation in cardiac anaphylaxis: histamine release and associated inotropic and chronotropic effects. .  246. 1988
• Dual action of morphine on fetal breathing movements. .  245. 1988
• Negative inotropic effect of platelet-activating factor: association with a decrease in intracellular sodium activity. .  245. 1988
• Cerebral metabolic interactions between thyroid state and imipramine in the rat. .  244. 1988
• Negative inotropic effect of platelet-activating factor on human myocardium: a pharmacological study. .  243. 1987
• Human postjunctional alpha-1 and alpha-2 adrenoceptors: differential distribution in arteries of the limbs. .  241. 1987
• Pharmacodynamic supersensitivity and opioid receptor upregulation in the mouse. .  239. 1986
• Effect of PGD2 on cardiac contractility: a negative inotropism secondary to coronary vasoconstriction conceals a primary positive inotropic action. .  237. 1986
• Depression of contractile responses in rat aorta by spontaneously released endothelium-derived relaxing factor. .  237. 1986
• Phosphodiesterase inhibitors induce endothelium-dependent relaxation of rat and rabbit aorta by potentiating the effects of spontaneously released endothelium-derived relaxing factor. .  237. 1986
• Pharmacokinetics and pharmacodynamics of subcutaneous naltrexone pellets in the rat. .  237. 1986
• Mechanism of tubular uptake on human growth hormone in perfused rat kidneys. .  236. 1986
• Pharmacokinetics and pharmacodynamics of subcutaneous morphine pellets in the rat. .  235. 1985
• Nimodipine and inhibition of alpha adrenergic activation of the isolated canine saphenous vein. .  234. 1985
• Blockade of endothelium-dependent and glyceryl trinitrate-induced relaxation of rabbit aorta by certain ferrous hemoproteins. .  233. 1985
• Selective blockade of endothelium-dependent and glyceryl trinitrate-induced relaxation by hemoglobin and by methylene blue in the rabbit aorta. .  232. 1985
• Adenosine selectively attenuates H2- and beta-mediated cardiac responses to histamine and norepinephrine: an unmasking of H1- and alpha-mediated responses. .  231. 1984
• Characterization of postjunctional alpha-1 and alpha-2 adrenoceptors activated by exogenous or nerve-released norepinephrine in the canine saphenous vein. .  230. 1984
• Negative inotropic effect of leukotrienes: leukotrienes C4 and D4 inhibit calcium-dependent contractile responses in potassium-depolarized guinea-pig myocardium. .  230. 1984
• Differences in d-[3H]lysergic acid diethylamide binding in mouse cortex and hippocampus in vivo and in vitro revealed by radioautography and rapid filtration studies. .  229. 1984
• Pharmacological characterization of the postsynaptic alpha adrenoceptors in vascular smooth muscle from canine and rat mesenteric vascular beds. .  229. 1984
• Tissue distribution and disposition of tin-protoporphyrin, a potent competitive inhibitor of heme oxygenase. .  228. 1984
• Discriminant effects of behaviorally active and inactive analogs of phencyclidine on membrane electrical excitability. .  228. 1984
• Reduction of ventricular fibrillation threshold by histamine: resolution into separate H1- and H2-mediated components. .  223. 1982
• Antinociceptive activity and toxicity of meperidine and normeperidine in mice. .  223. 1982
• 3,4-diaminopyridine alters acetylcholine metabolism and behavior during hypoxia. .  222. 1982
• Nicotinic-catecholaminergic interactions in rat brain: evidence for cholinergic nicotinic and muscarinic interactions with hypothalamic epinephrine. .  221. 1982
• Leukotrienes C4, D4 and E4: effects on human and guinea-pig cardiac preparations in vitro. .  221. 1982
• Pharmacodynamics of subcutaneously administered diacetylmorphine, 6-acetylmorphine and morphine in mice. .  218. 1981
• Antiarrhythmic effect of manganese chloride in infarcted dogs with observations on the dose-related response of heart rate and ventricular pressure. .  218. 1981
• Impairment of behavior and acetylcholine metabolism in thiamine deficiency. .  217. 1981
• Methadone: radioimmunoassay and pharmacokinetics in the rat. .  217. 1981
• Thromboxane and prostacyclin release during cardiac immediate hypersensitivity reactions in vitro. .  217. 1981
• Tyrosine hydroxylase: studies on the phosphorylation of a purified preparation of the brain enzyme by the cyclic AMP-dependent protein kinase. .  216. 1981
• The cardiac pharmacology of tiotidine (LCL 125, 211): a new histamine H2-receptor antagonist. .  214. 1980
• The cardiac effects of prostaglandins and their modification by the prostaglandin antagonist N-0164. .  214. 1980
• Renal tubular secretion of meperidine by the fetal lamb. .  213. 1980
• Localization and quantitation of lithium in rat tissue following intraperitoneal injections of lithium chloride. II. Brain. .  212. 1980
• Urinary excretion of meperidine by the fetal lamb. .  209. 1979
• Actions at neuromuscular and esteratic cholinoceptive sites of some phenylene diacryloyl bis-cholinium esters. .  208. 1979
• Histamine-induced negative inotropism: mediation by H1-receptors. .  206. 1978
• Meperidine pharmacokinetics in the maternal-fetal unit. .  206. 1978
• Modification of the effects of histamine and norepinephrine on the sinoatrial node pacemaker by potassium and calcium. .  204. 1978
• Tryptoline inhibition of serotonin uptake in rat forebrain homogenates. .  198. 1976
• Monoamine oxidase inhibition and the induction of ponto-geniculo-occipital wave activity by reserpine in the cat. .  197. 1976
• Dopamine synthesis in rat brain striatal synaptosomes. I. Correlations between veratridine-induced synthesis stimulation and endogenous dopamine release. .  197. 1976
• Dopamine synthesis in rat brain striatal synaptosomes. II. Dibutyryl cyclic adenosine 3':5'-monophosphoric acid and 6-methyltetrahydropterine-induced synthesis increases without an increase in endogenous dopamine release. .  197. 1976
• Intestinal smooth muscle contraction and the effects of cadmium and A23187. .  194. 1975
• Cardiac histamine-ouabain interaction: potentiation by ouabain of the arrhythmogenic effects of histamine. .  192. 1975
• Brain norepinephrine metabolism and shock-induced fighting behavior in rats: differential effects of shock and fighting on the neurochemical response to a common footshock stimulus. .  190. 1974
• A comparison of psychotomimetic drug effects on rat brain norepinephrine metabolism. .  189. 1974
• Differences in inducibility of cutaneous and hepatic drug metabolizing enzymes and cytochrome P-450 by polychlorinated biphenyls and 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT). .  188. 1974
• Drug stimulation of -aminolevulinic acid synthetase and cytochrome P-450 in vivo in chick embryo liver. .  185. 1973
• Effects of exogenous and immunologically released histamine on the isolated heart: a quantitative comparison. .  182. 1972
• The tubular transport and metabolism of morphine-N-methyl-C14 by the chicken kidney. .  157. 1967
• Effects of melatonin and related compounds on the release of glycerol from rat adipose tissue in vitro. .  152. 1966
• STRESS-INDUCED RELEASE OF BRAIN NOREPINEPHRINE AND ITS INHIBITION BY DRUGS. .  143. 1964
• The synthesis and estimation of N-C14-methyl labeled levorphanol and its biological disposition in the monkey, dog and rat. .  124. 1958
• Moving the Journal of Pharmacology and Experimental Therapeutics Forward to Address the Needs of Our Authors and Editors-Editorial. .  388. 2024
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We have just received the first number of a new journal, the Journal of Pharmacology and Experimental Therapeutics , edited, with the assistance of a number of associate editors, by J. J. Abel, the distinguished professor of pharmacology at Johns Hopkins University. This journal is devoted to the publication of original investigations in pharmacology, experimental therapeutics and closely related subjects. The publication of a journal of this character is a most encouraging indication of the rapid growth of pharmacology in this country. It is but comparatively recently that pharmacology has received recognition here as a separate branch of medical science. Both in the medical schools and in the government laboratories the work of the pharmacologist has been done by men who had no special preparation for the work—in the medical schools by clinicians, in the government laboratories by chemists.

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Bibliographic Information

Williams & Wilkins, 1909-2011

• Vol. 1 (1909/1910)-v. 339, no. 3 (Dec. 2011)

J. pharmacol. exp. ther (Print)

The Journal of pharmacology and experimental therapeutics (Print)

Access to Electronic Resource  79  items

v.1 1909-1910 1910

v.1 (1909-10) 1910

v.1 (1909-June 1910) 1910

v.2 1910-1911 1911

v.1-2(1909-1911) 1911

v.2 (1910-11) 1911

v.2 (Aug 1910-July 1911) 1911

v.3 1911-1912 1912

v.3 (1911-12) 1912

v.3-4 1911-1913 1913

v.4 (1912-13) 1913

v.5 (1913-14) 1914

v.5-6 1913-1915 1915

v.7 1915 1915

v.6 (1914-15) 1915

v.7 (1915) 1915

v.8 1916 1916

v.007-008 yr.1915-16 1916

v.8 (1916) 1916

c.1 v.9 1917 1917

v.9 (1916-1917) 1917

v.9 1916-1917 1917

v.9 1916-17 1917

v.9 1917 1917

v.9 (1916-17) 1917

v.10 (1917) 1917

v.10 (1917-1918) 1918

v.11 (1918) 1918

v.10 1917-1918 1918

v.11 1918 1918

v.10 1917-18 1918

v.9-10(1916-1918) 1918

v.009-010 yr.1917-18 1918

v.10 (1917-18) 1918

c.1 v.12 1919 1919

v.12 (1918-1919) 1919

v.13 (1919) 1919

v.12 1918-1919 1919

v.13 1919 1919

v.12 1918-19 1919

v.011-012 yr.1918-19 1919

v.12 (1919) 1919

v.012 yr.1919 1919

v.14 (1919-1920) 1920

v.15 (1920) 1920

v.14 1919-1920 1920

v.15 1920 1920

v.14 1919-20 1920

v.013-014 yr.1919-20 1920

v.14 (1919-20) 1920

v.16 (1920-1921) 1921

v.17 (1921) 1921

v.16 1920-1921 1921

v.17 1921 1921

v.15-16 1920-21 1921

v.16 (1920-21) 1921

v.16 (1921) 1921

v.18 (1921) 1921

v.19 (1922) 1922

v.18 1921-1922 1922

v.19 1922 1922

v.17-18 1921-22 1922

v.18 (1921-22) 1922

v.20 1922-1923 1923

v.21-22(1923) 1923

v.20 (1922-23) 1923

index v.1-20 (1910-23) 1923

v.21 (1923) 1923

v.22 (1923) 1923

v.23 (1923) 1923

v.23 1924 1924

v.24 1924-1925 1925

v.25 1925 1925

v.25 (1925) 1925

v.26 1925-1926 1926

v.24 (1925-26) 1926

v.27 (1926) 1926

v.28 (1926) 1926

v.31 (1927) 1927

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愛知学院大学 歯学・薬学図書館情報センター 歯薬図 1941-2007

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Okayama University Institute of Plant Science and Resources Branch Library 植物研図 1909-1953 203.2/J

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Okayama University Library 附属図 1946-2004 ZF49/J

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Okayama University Library, Shikata Branch Library 鹿田図 1909-2004

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Obihiro University of Agriculture and Veterinary Medicine Library 図 1965-2005

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Faculty of Medicine Branch, Kagawa University Library 1976-2005 QV

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Kanazawa University Library 自然図自動書庫 1909-2006

Kanazawa University Medical Library 医学図雑誌 1990-2003

川崎医科大学 附属図書館 1971-2004

関西医科大学 附属図書館 本館 1951-2007

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Kwansei Gakuin University Library 三雑 2004-2011 610

北里大学 医学図書館 1980-1998

北里大学 獣医学部図書館 1959-2006

北里大学 図書館 白金分館 1951-1970

Kyushu University of Health and Welfare 1999-2007

288-316, 317(1-2), 318-319

Kyushu Kyoritsu University Library 図 1964-1988

143-183, 196-247

九州歯科大学 附属図書館 図 1956-2009

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Kyushu University Medical Library 医分 1909-2003

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Kyushu University Medical Library 生医研別府 1972-1995

九州女子大学・九州女子短期大学 附属図書館 2008-2011

京都大学 大学院薬学研究科・薬学部 図書室 薬図 1941-2001

Kyoto Pharmaceutical University Library 1920-2011 P-49||JPHAOET

杏林大学 医学図書館 医図 1909-2011

1-179, 180(1-2), 181-185, 186(1-2), 189-339

The Medical Library, Kyoto University 医図 1909-2011 J||100

1-85, 87-93, 94(3-4), 95-152, 153(1, 3), 154-339

京都府立医科大学 附属図書館 図 1913-2006

5(1-5), 13(1-2, 4-5), 14-15, 16(1-2), 19-20, 21(1), 23-71, 98-319

近畿大学 医学部図書館 医図 1986-2011

Kindai University Central Library 中図 1909-1994 Z49-J4

岐阜大学 医学図書館 医分 2002-2003

岐阜大学 医学図書館 薬理 2003-2004

Gifu University Library 図畜産 1941-2001

71-72, 100-299

岐阜薬科大学 附属図書館 1966-2007

熊本大学 附属図書館 医学系分館 図書館 1919-2010

12-18, 20-72, 101-304, 312-335

熊本大学 附属図書館 薬学部分館 1957-2008

久留米大学 附属図書館 医学部分館 図書館 1953-2004

107-255(1-2), 256-311

久留米大学 附属図書館 医学部分館 講座 2005-2005

Medical Library of Gunma University 図書館 1949-2011

95(2), 96(), 97(), 98-294, 295(2-3), 296-339

Keio University Shinanomachi Media Center 1909-2011

1-80, 82-100, 101(2-4), 102-339

結核予防会結核研究所 図書室 1981-1995

公益財団法人 天理よろづ相談所 医学研究所 医学図書館 2006-2011

厚生労働省 国立医薬品食品衛生研究所 安全情報部図書係 1952-2011

高知大学 学術情報基盤図書館 医学部分館 1950-2011

100-104, 171-339

神戸学院大学 図書館 ポートアイランドキャンパス館 1959-2010 499

127-324, 325(2-3), 326-335

Kobe University Library for Medical Sciences 1948-2003 J-44 ; 294

94-139, 140(1, 3), 141-192, 193(2-3), 194-196, 197(2-3), 198-307

公立大学法人 福島県立医科大学 附属学術情報センター 図 1920-2007

15, 18-20, 30, 34, 36-53, 56-60, 62-67, 71-283, 284(2-3), 285-323

国立 がん研究センター 図書館 1962-1976

Library of National College of Nursing 1977-1998

National Institute for Environmental Studies 1997-1999

国立研究開発法人 国立がん研究センター 図書館 東分室 1987-1989

240-246, 248-251

国立研究開発法人 国立成育医療研究センター 図書館 1991-1997

256(2, 3), 257-279, 280(2, 3)

国立精神・神経医療研究センター 図書館 1985-2007

国立精神・神経医療研究センター 図書館 本館 1985-2007

Library, National Institute of Public Health 1968-1998

埼玉医科大学 附属図書館 埼医大図 1940-2009

埼玉医科大学 附属図書館 総合医療センター 2000-2003

埼玉県立がんセンター 図書館 1976-2010

Saga University Medical Library 1973-2003

184-236, 288-307

札幌医科大学 附属総合情報センター 図 1941-2011

73(3-4), 74(2-4), 75(3-4), 92, 93(1-2, 4), 95(2-3), 96(2-4), 97, 98(1-3), 99(1, 3-4), 100-240, 241(1, 3), 242-339

産業医科大学 図書館 1958-2003 /

滋賀医科大学 附属図書館 図 1956-2005

116-283, 288-290, 291(1-2), 296-315

University of Shizuoka Kusanagi Library 1956-2005 491.05||J-2

National Institutes of Natural Sciences Okazaki Library and Information Center 図 1909-2015

Shimane University Medical Library 1960-2007

就実大学 図書館 2002-2004

昭和大学 図書館 1968-2011

昭和薬科大学 図書館 1972-2010

信州大学 附属図書館 医学部図書館 1915-2011

7-9, 11-19, 21(1-4, 6), 22-26, 91-92, 96-339

自治医科大学 図書館 1965-2008

147-303, 304(1-2), 305-327

Joetsu University of Education Library 1955-1969 4

城西大学 水田記念図書館 自然系 1948-2007

Sophia University Library 中央 1991-2009 Za22:J82680

摂南大学 図書館 枚方分館 分館 1909-2002 491.505||J

第一薬科大学 図書館 1967-1998

千葉科学大学 図書館 図 2003-2007

千葉大学 附属図書館 亥鼻分館 亥分 1909-2003

Osaka Institute of Public Health 図 1964-1995 Y46003

143-149, 150(1-2), 151-271, 272(1)

University of Tsukuba Library, Medical Library 1909-2009 洋 J

鶴見大学 図書館 1909-2011

帝京科学大学 附属図書館 東京西図書館 1997-2011

帝京大学 医学総合図書館 1951-2010 (intend)

Tokai University Isehara Campus Library 2001-2009

東京医科歯科大学 図書館 図 1909-2011 一括

1-72, 76, 79-206, 208-252, 256-311, 324-339

東京医科大学 図書館分館 図 1960-2011

Tokyo Institute of Technology Suzukakedai Library 1977-2002

東京歯科大学 図書館 1956-2010 400

116, 117(1, 3-4), 118-335

Academic Information Center, The Jikei University School of Medicine 1909-2011

東京女子医科大学 図書館 本館 2003-2010

Medical Library, The University of Tokyo 図書 1981-2011

東京大学 柏図書館 書庫 1909-1999

University Library for Agricultural and Life Sciences, The University of Tokyo 図 1909-2011

1-52, 54-339

Graduate School of Pharmaceutical Sciences, Pharmaceutical Sciences Library, University of Tokyo 図書 1991-2002

東京都医学総合研究所 図書室 1960-2008

129-323, 324(1-2)

東京農業大学 生物産業学部図書館 生産図 1989-1990

248-250, 252(3), 253(1)

Tokyo University of Agriculture 図 1971-2011 615||J86

Tokyo University of Agriculture and Technology Library, Fuchu Library 1965-1992

147-170, 172-263

東京薬科大学 図書館 1954-2009

110-207, 208(), 209-331

東京理科大学 野田図書館 保存書庫 1986-2008

236-315, 320-327

東京理科大学 野田図書館 薬学部 2009-2011

東京理科大学 野田図書館 野図 1961-2006

131-263, 316-319

東邦大学 医学メディアセンター 1975-2011

東邦大学 習志野メディアセンター 1962-2005

東北医科薬科大学 附属図書館 1941-2011

71-103, 107-149, 150(1-2), 151-339

Tohoku University Medical Library 図 1909-2011

1-95, 96(3-4), 97-218, 219(1), 220-339

徳島大学 附属図書館 蔵本分館 1950-2005

98-116, 117(1-3), 118-315

徳島文理大学 図書館 図 1909-2011

1-103, 155-339

Tottori University Library 図 1981-1985

Tottori University Medical Library 図 1950-2005

University of Toyama Library, Medical and Pharmaceutical Library 図 1926-2011 QV34

27-46, 101-339

独立行政法人 労働安全衛生総合研究所 (登戸地区図書館) 登戸図 1972-2002

獨協医科大学 図書館 1950-2011

98-321, 322(2-3), 323-339

中村学園大学 図書館 1992-2011

260-270, 271(3), 272-331, 332(2-3), 333-339

Nagaoka Universtiy of Technology Library 1975-2001

Nagasaki University Library Central Library 中央館 1954-2004

110-123, 128-311

Nagasaki University Medical library 1949-2006

Nagasaki University Medical library 薬理1 1994-1995

長野県看護大学 付属図書館 図 1998-2002

284-295, 297-303

名古屋市立大学 総合情報センター 川澄分館 1980-2007

212-319, 320(1-2)

名古屋市立大学 総合情報センター 田辺通分館 1965-2011

Nagoya University Library 農雑誌 1976-1992

Nagoya University Library 中央雑 1954-1975

Nagoya University Library 医分館 1909-2007

1, 3-46, 48, 51-55, 59-275, 276(1), 277-323

奈良県立医科大学 附属図書館 1916-2002 P-Jou

8-13, 91-300, 301(1)

新潟大学 附属図書館 旭町分館 旭分 1909-2011 490

新潟薬科大学 附属図書館 薬学 1960-2006

日本医師会 医学図書館 1954-2011

日本歯科大学 生命歯学部図書館 1954-2004

日本獣医生命科学大学 付属図書館 1963-2011 491.5

Nihon University School of Medicine 1F 1995-2011

272-313, 314(1-2), 315-339

Nihon University School of Medicine B2 1952-1994

104-154, 155(1-2), 156-271

日本大学 薬学部図書館 1941-2011 薬34

71-103, 139-165, 171-339

農業・食品産業技術総合研究機構 動物衛生研究部門 図書室 1951-1997

101-109, 131-280

Agriculture, Forestry and Fisheries Research Information Technology Center (AFFRIT) 1937-1939

59-61, 62(1-3), 63-67

東日本電信電話株式会社 関東病院 図書館 1995-1999

兵庫医科大学 神戸キャンパス図書館 図 2007-2011

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Hirosaki University Medical Library 1941-2010

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広島国際大学 図書館 呉分館 呉図 2003-2005

Hiroshima University Central Library, Interlibrary Loan 図・自動書庫 1995-2004

Hiroshima University Central Library, Interlibrary Loan 特殊 1941-1994

71-119, 120(1-3), 121(2-4), 122-271

福井大学 附属図書館 医学図書館 1940-2011

68-291, 300-339

University of Teacher Education Fukuoka Library 図 1975-2005

192-257, 258(1, 3), 259-289, 290(1-2), 291-292, 293(1), 294-300, 302-315

福岡歯科大学 情報図書館 1909-2006

福岡大学 図書館 1941-2011 490

福岡大学 図書館 医学部分館 1909-2009 QV

福山大学 附属図書館 1971-1987

福山大学 附属図書館 分館 1988-2011

藤田医科大学 図書館 1991-2009

放送大学 附属図書館 1994-1998

268-279, 280(1-2), 281-287

北陸大学 図書館 薬学部分館 薬学 1945-2007

星薬科大学 図書館 1941-2011

北海道大学 医学研究科・医学部図書館 図書 1909-2005

北海道大学 大学院歯学研究院・大学院歯学院・歯学部図書室 図書 1969-1998

北海道大学 大学院獣医学研究院図書室 図書 1909-1998

1-97, 99-107, 108(3-4), 109-123, 124(2-4), 125-287

北海道医療大学 総合図書館 総図 1972-2011

防衛省防衛医科大学校 図書館 1909-2007

Matsumoto Dental University Library 図 1971-2008

三重大学 医学部図書館 医学科 1991-2006 49

256-290, 291(1-2), 292(2-3), 293-319

Mie Univ. Library 図 1976-1990 49

University of Miyazaki, Library 図 1960-2008 M||JournalPharmacologyExper

128-287, 296-327

明海大学 歯学部 メデイアセンター(図書館) 1961-2002

明治薬科大学 図書館 1941-2008

名城大学 附属図書館 薬学部分館 薬 1941-2008

安田女子大学 図書館 2005-2010

山形大学 医学部図書館 1986-1986

General Library Yamaguchi University 1978-2001

山口大学 図書館 医学部図書館 1950-2004

University of Yamanashi Library, Medical Branch 図 1966-2011 QV

153, 156, 161-162, 208-336, 337(2-3), 338-339

横浜市立大学 医学情報センター 1948-2006

92-94, 101-299, 300(2-3), 301(1), 303(2), 308, 312, 316, 318(1)

横浜市立大学 学術情報センター 1991-2004 P49||14

256-288, 296(3), 298(3), 300(1), 301-302, 303(1-2), 304(2), 308

横浜薬科大学 図書館 2006-2011

316(3), 317-320, 321(1, 3), 322-327, 328(1-2), 330(3), 334(3), 335(1, 3), 336, 337(1-2), 338, 339(1-2)

酪農学園大学 附属図書館 図 1969-2011

166-182, 184-339

琉球大学 附属図書館 医学部分館 1976-2003

196-267, 268(2-3), 269-307

量子科学技術研究開発機構 1959-2006

125-166, 167(2), 168-319

和歌山県立医科大学 図書館 紀三井寺館 図 1950-2004

98-302, 304-311

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• NCID AA00704632
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Anti-inflammatory Properties of Cannabidiol, a Nonpsychotropic Cannabinoid, in Experimental Allergic Contact Dermatitis

Affiliations.

• 1 Endocannabinoid Research Group, Istituto di Chimica Biomolecolare, Consiglio Nazionale delle Ricerche, Pozzuoli, Napoli, Italy (S.P., R.V., M.A., V.D.); Epitech Group SpA, Saccolongo, Padova, Italy (S.P., M.A.); and Dipartimento di Farmacologia Sperimentale, Università di Napoli "Federico II", Napoli, Italy (M.V., T.I.).
• 2 Endocannabinoid Research Group, Istituto di Chimica Biomolecolare, Consiglio Nazionale delle Ricerche, Pozzuoli, Napoli, Italy (S.P., R.V., M.A., V.D.); Epitech Group SpA, Saccolongo, Padova, Italy (S.P., M.A.); and Dipartimento di Farmacologia Sperimentale, Università di Napoli "Federico II", Napoli, Italy (M.V., T.I.) [email protected].
• PMID: 29632236
• DOI: 10.1124/jpet.117.244368

Phytocannabinoids modulate inflammatory responses by regulating the production of cytokines in several experimental models of inflammation. Cannabinoid type-2 (CB 2 ) receptor activation was shown to reduce the production of the monocyte chemotactic protein-2 (MCP-2) chemokine in polyinosinic-polycytidylic acid [poly-(I:C)]-stimulated human keratinocyte (HaCaT) cells, an in vitro model of allergic contact dermatitis (ACD). We investigated if nonpsychotropic cannabinoids, such as cannabidiol (CBD), produced similar effects in this experimental model of ACD. HaCaT cells were stimulated with poly-(I:C), and the release of chemokines and cytokines was measured in the presence of CBD or other phytocannabinoids (such as cannabidiol acid, cannabidivarin, cannabidivarinic acid, cannabichromene, cannabigerol, cannabigerolic acid, cannabigevarin, tetrahydrocannabivarin, and tetrahydrocannabivarinic acid) and antagonists of CB 1 , CB 2 , or transient receptor potential vanilloid type-1 (TRPV1) receptors. HaCaT cell viability following phytocannabinoid treatment was also measured. The cellular levels of endocannabinoids [anandamide (AEA), 2-arachidonoylglycerol] and related molecules (palmitoylethanolamide, oleoylethanolamide) were quantified in poly-(I:C)-stimulated HaCaT cells treated with CBD. We show that in poly-(I:C)-stimulated HaCaT cells, CBD elevates the levels of AEA and dose-dependently inhibits poly-(I:C)-induced release of MCP-2, interleukin-6 (IL-6), IL-8, and tumor necrosis factor- α in a manner reversed by CB 2 and TRPV1 antagonists 6-iodopravadoline (AM630) and 5'-iodio-resiniferatoxin (I-RTX), respectively, with no cytotoxic effect. This is the first demonstration of the anti-inflammatory properties of CBD in an experimental model of ACD.

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