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Article ; Online: Tobacco addiction and the dysregulation of brain stress systems.

Bruijnzeel, Adrie W

2012 Volume 36, Issue 5, Page(s) 1418–1441

Abstract: Tobacco is a highly addictive drug and is one of the most widely abused drugs in the world. The first part of this review explores the role of stressors and stress-associated psychiatric disorders in the initiation of smoking, the maintenance of smoking, ...

Abstract	Tobacco is a highly addictive drug and is one of the most widely abused drugs in the world. The first part of this review explores the role of stressors and stress-associated psychiatric disorders in the initiation of smoking, the maintenance of smoking, and relapse after a period of abstinence. The reviewed studies indicate that stressors facilitate the initiation of smoking, decrease the motivation to quit, and increase the risk for relapse. Furthermore, people with depression or an anxiety disorder are more likely to smoke than people without these disorders. The second part of this review describes animal studies that investigated the role of brain stress systems in nicotine addiction. These studies indicate that corticotropin-releasing factor, Neuropeptide Y, the hypocretins, and norepinephrine play a pivotal role in nicotine addiction. In conclusion, the reviewed studies indicate that smoking briefly decreases subjective stress levels but also leads to a further dysregulation of brain stress systems. Drugs that decrease the activity of brain stress systems may diminish nicotine withdrawal and improve smoking cessation rates.
MeSH term(s)	Animals ; Corticotropin-Releasing Hormone/physiology ; Disease Models, Animal ; Humans ; Hypothalamo-Hypophyseal System/physiopathology ; Intracellular Signaling Peptides and Proteins/physiology ; Mental Disorders/complications ; Mental Disorders/physiopathology ; Mental Disorders/psychology ; Neuropeptide Y/physiology ; Neuropeptides/physiology ; Norepinephrine/physiology ; Orexins ; Pituitary-Adrenal System/physiopathology ; Tobacco Use Disorder/complications ; Tobacco Use Disorder/physiopathology ; Tobacco Use Disorder/psychology
Chemical Substances	Intracellular Signaling Peptides and Proteins ; Neuropeptide Y ; Neuropeptides ; Orexins ; Corticotropin-Releasing Hormone (9015-71-8) ; Norepinephrine (X4W3ENH1CV)
Language	English
Publishing date	2012-03-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	282464-4
ISSN	1873-7528 ; 0149-7634
ISSN (online)	1873-7528
ISSN	0149-7634
DOI	10.1016/j.neubiorev.2012.02.015
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Zs.A 1371: Show issues

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Article ; Online: kappa-Opioid receptor signaling and brain reward function.

Bruijnzeel, Adrie W

Brain research reviews

2009 Volume 62, Issue 1, Page(s) 127–146

Abstract: The dynorphin-like peptides have profound effects on the state of the brain reward system and human and animal behavior. The dynorphin-like peptides affect locomotor activity, food intake, sexual behavior, anxiety-like behavior, and drug intake. ... ...

Abstract	The dynorphin-like peptides have profound effects on the state of the brain reward system and human and animal behavior. The dynorphin-like peptides affect locomotor activity, food intake, sexual behavior, anxiety-like behavior, and drug intake. Stimulation of kappa-opioid receptors, the endogenous receptor for the dynorphin-like peptides, inhibits dopamine release in the striatum (nucleus accumbens and caudate putamen) and induces a negative mood state in humans and animals. The administration of drugs of abuse increases the release of dopamine in the striatum and mediates the concomitant release of dynorphin-like peptides in this brain region. The reviewed studies suggest that chronic drug intake leads to an upregulation of the brain dynorphin system in the striatum and in particular in the dorsal part of the striatum/caudate putamen. This might inhibit drug-induced dopamine release and provide protection against the neurotoxic effects of high dopamine levels. After the discontinuation of chronic drug intake these neuroadaptations remain unopposed which has been suggested to contribute to the negative emotional state associated with drug withdrawal and increased drug intake. kappa-Opioid receptor agonists have also been shown to inhibit calcium channels. Calcium channel inhibitors have antidepressant-like effects and inhibit the release of norepinephrine. This might explain that in some studies kappa-opioid receptor agonists attenuate nicotine and opioid withdrawal symptomatology. A better understanding of the role of dynorphins in the regulation of brain reward function might contribute to the development of novel treatments for mood disorders and other disorders that stem from a dysregulation of the brain reward system.
MeSH term(s)	Animals ; Brain/metabolism ; Dynorphins/metabolism ; Humans ; Receptors, Opioid, kappa/metabolism ; Reward ; Substance Withdrawal Syndrome/metabolism ; Substance-Related Disorders/metabolism
Chemical Substances	Receptors, Opioid, kappa ; Dynorphins (74913-18-1)
Language	English
Publishing date	2009-10-02
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	423722-5
ISSN	1872-6321 ; 0165-0173
ISSN (online)	1872-6321
ISSN	0165-0173
DOI	10.1016/j.brainresrev.2009.09.008
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Zs.A 1506: Show issues

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Article ; Online: Animal models of nicotine withdrawal: intracranial self-stimulation and somatic signs of withdrawal.

Bauzo, Rayna M / Bruijnzeel, Adrie W

Methods in molecular biology (Clifton, N.J.)

2012 Volume 829, Page(s) 257–268

Abstract: Tobacco addiction is one of the leading causes of preventable death worldwide. Despite the negative health outcomes of tobacco use and a desire to quit, there is a low success rate of maintaining abstinence. Nicotine, the main psychoactive component of ... ...

Abstract	Tobacco addiction is one of the leading causes of preventable death worldwide. Despite the negative health outcomes of tobacco use and a desire to quit, there is a low success rate of maintaining abstinence. Nicotine, the main psychoactive component of tobacco smoke, is mildly rewarding and maintains smoking behavior. Nicotine withdrawal induces somatic symptoms that may contribute to smoking behavior. However, it has been hypothesized that the negative affective signs are of greater motivational significance in contributing to relapse and continued tobacco use than the somatic symptoms of nicotine withdrawal (Markou and Koob (Eds.) Intracranial self-stimulation thresholds as a measure of reward, Vol. 2, Oxford University Press, New York, 1993; Koob et al. Semin Neurosci 5: 351-358, 1993). Intracranial self-stimulation (ICSS) has been established as a method to assess the bivalent properties of nicotine exposure and withdrawal from acute and chronic nicotine administration. Thus, ICSS provides a means to measure the negative affective aspects of nicotine withdrawal in animal models and may contribute to the understanding of the neurobiological bases of nicotine dependence and the development of effective treatment strategies to facilitate nicotine abstinence.
MeSH term(s)	Animals ; Behavior, Animal ; Deep Brain Stimulation/methods ; Male ; Models, Animal ; Nicotine/administration & dosage ; Nicotine/adverse effects ; Rats ; Self Administration ; Smoking ; Substance Withdrawal Syndrome ; Substance-Related Disorders ; Tobacco Use Disorder
Chemical Substances	Nicotine (6M3C89ZY6R)
Language	English
Publishing date	2012
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-61779-458-2_16
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Article ; Online: Stimulation of α2-adrenergic receptors in the central nucleus of the amygdala attenuates stress-induced reinstatement of nicotine seeking in rats.

Yamada, Hidetaka / Bruijnzeel, Adrie W

Neuropharmacology

2010 Volume 60, Issue 2-3, Page(s) 303–311

Abstract: Tobacco addiction is a chronic disorder that is characterized by craving for tobacco products, withdrawal upon smoking cessation, and relapse after periods of abstinence. Previous studies demonstrated that systemic administration of α2-adrenergic ... ...

Abstract	Tobacco addiction is a chronic disorder that is characterized by craving for tobacco products, withdrawal upon smoking cessation, and relapse after periods of abstinence. Previous studies demonstrated that systemic administration of α2-adrenergic receptor agonists attenuates stress-induced reinstatement of drug seeking in rats. The aim of the present experiments was to investigate the role of noradrenergic transmission in the central nucleus of amygdala (CeA) in stress-induced reinstatement of nicotine seeking. Rats self-administered nicotine for 14-16 days and then nicotine seeking was extinguished by substituting saline for nicotine. The effect of the intra-CeA infusion of the α2-adrenergic receptor agonists clonidine and dexmedetomidine, the nonselective β1/β2-adrenergic receptor antagonist propranolol, and the α1-adrenergic receptor antagonist prazosin on stress-induced reinstatement of nicotine seeking was investigated. In all the experiments, exposure to footshocks reinstated extinguished nicotine seeking. The administration of clonidine or dexmedetomidine into the CeA attenuated stress-induced reinstatement of nicotine seeking. The administration of propranolol or prazosin into the CeA did not affect stress-induced reinstatement of nicotine seeking. Furthermore, intra-CeA administration of clonidine or dexmedetomidine did not affect operant responding for food pellets. This suggests that the effects of clonidine and dexmedetomidine on stress-induced reinstatement of nicotine seeking were not mediated by motor impairments or sedation. Taken together, these findings indicate that stimulation of α2-adrenergic receptors, but not blockade of α1 or β-adrenergic receptors, in the CeA attenuates stress-induced reinstatement of nicotine seeking. These findings suggest that α2-adrenergic receptor agonists may at least partly attenuate stress-induced reinstatement of nicotine seeking by stimulating α2-adrenergic receptors in the CeA.
MeSH term(s)	Adrenergic alpha-2 Receptor Agonists/pharmacology ; Adrenergic alpha-2 Receptor Agonists/therapeutic use ; Amygdala/drug effects ; Amygdala/metabolism ; Animals ; Behavior, Addictive/etiology ; Behavior, Addictive/metabolism ; Behavior, Addictive/prevention & control ; Conditioning, Operant/drug effects ; Conditioning, Operant/physiology ; Male ; Nicotine/administration & dosage ; Rats ; Rats, Wistar ; Receptors, Adrenergic, alpha-2/metabolism ; Self Administration ; Stress, Psychological/complications ; Stress, Psychological/drug therapy ; Stress, Psychological/metabolism ; Tobacco Use Disorder/etiology ; Tobacco Use Disorder/metabolism ; Tobacco Use Disorder/prevention & control
Chemical Substances	Adrenergic alpha-2 Receptor Agonists ; Receptors, Adrenergic, alpha-2 ; Nicotine (6M3C89ZY6R)
Language	English
Publishing date	2010-09-18
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2010.09.013
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Article ; Online: Anorexic effects of intra-VTA leptin are similar in low-fat and high-fat-fed rats but attenuated in a subgroup of high-fat-fed obese rats.

Bruijnzeel, Adrie W / Qi, Xiaoli / Corrie, Lu W

Pharmacology, biochemistry, and behavior

2012 Volume 103, Issue 3, Page(s) 573–581

Abstract: Leptin is an adiposity hormone that plays an important role in regulating food intake and energy homeostasis. This study investigated the effects of a high-fat (HF) and a low-fat, high-carbohydrate/sugar (LF) diet on leptin sensitivity in the ventral ... ...

Abstract	Leptin is an adiposity hormone that plays an important role in regulating food intake and energy homeostasis. This study investigated the effects of a high-fat (HF) and a low-fat, high-carbohydrate/sugar (LF) diet on leptin sensitivity in the ventral tegmental area (VTA) in rats. The animals were exposed to a HF or LF diet for 16 weeks. Then the effects of intra-VTA leptin (150 and 500 ng/side, unilateral dose) on food intake and body weights were investigated while the animals were maintained on the HF or LF diet. Long-term exposure to the HF or LF diet led to similar body weight gain in these groups. The HF-fed animals consumed a smaller amount of food by weight than the LF-fed animals but both groups consumed the same amount of calories. The bilateral administration of leptin into the VTA decreased food intake (72 h) and body weights (48 h) to a similar degree in the HF and LF-fed animals. When the HF-fed animals were ranked by body weight gain it was shown that the diet-induced obese rats (HF-fed DIO, upper quartile for weight gain) were less sensitive to the effects of leptin on food intake and body weights than the diet-resistant rats (HF-fed DR, lower quartile for weight gain). A control experiment with fluorescent Cy3-labeled leptin showed that leptin did not spread beyond the borders of the VTA. This study indicates that leptin sensitivity in the VTA is the same in animals that are exposed to a HF or LF diet. However, HF-fed DIO rats are less sensitive to the effects of leptin in the VTA than HF-fed DR rats. Leptin resistance in the VTA might contribute to overeating and weight gain when exposed to a HF diet.
MeSH term(s)	Animals ; Anorexia/chemically induced ; Appetite Depressants/administration & dosage ; Appetite Depressants/pharmacology ; Body Weight/drug effects ; Diet, Fat-Restricted ; Diet, High-Fat ; Dietary Carbohydrates/pharmacology ; Dietary Fats/pharmacology ; Eating/drug effects ; Energy Intake/drug effects ; Leptin/administration & dosage ; Leptin/antagonists & inhibitors ; Leptin/pharmacology ; Male ; Microinjections ; Obesity/chemically induced ; Obesity/physiopathology ; Rats ; Rats, Sprague-Dawley ; Ventral Tegmental Area/drug effects
Chemical Substances	Appetite Depressants ; Dietary Carbohydrates ; Dietary Fats ; Leptin
Language	English
Publishing date	2012-10-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	191042-5
ISSN	1873-5177 ; 0091-3057
ISSN (online)	1873-5177
ISSN	0091-3057
DOI	10.1016/j.pbb.2012.10.012
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Zs.A 1060: Show issues

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Article: The role of corticotropin-releasing factor-like peptides in cannabis, nicotine, and alcohol dependence.

Bruijnzeel, Adrie W / Gold, Mark S

Brain research. Brain research reviews

2005 Volume 49, Issue 3, Page(s) 505–528

Abstract: The corticotropin-releasing factor (CRF)-like peptides, which include the mammalian peptides CRF, urocortin 1, urocortin 2, and urocortin 3, play an important role in orchestrating behavioral and physiological responses that may increase an organism's ... ...

Abstract	The corticotropin-releasing factor (CRF)-like peptides, which include the mammalian peptides CRF, urocortin 1, urocortin 2, and urocortin 3, play an important role in orchestrating behavioral and physiological responses that may increase an organism's chance of survival when confronted with internal or external stressors. There is, however, evidence that a chronic overactivity of brain CRF systems under basal conditions may play a role in the etiology and maintenance of psychiatric disorders such as depression and anxiety disorders. In addition, there is evidence of a role for CRF-like peptides in acute and protracted drug abstinence syndromes and relapse to drug-taking behavior. This review focuses on the role of CRF-like peptides in the negative affective state associated with acute and protracted withdrawal from three widely abused drugs, cannabis, nicotine, and alcohol. In addition, we discuss the high comorbidity between stress-associated psychiatric disorders and drug dependence. A better understanding of the brain stress systems that may underlie psychiatric disorders, acute and protracted drug withdrawal, and relapse to drug-taking behavior may help in the development of new and improved pharmacotherapies for these widespread psychiatric disorders.
MeSH term(s)	Alcoholism/physiopathology ; Animals ; Corticotropin-Releasing Hormone/physiology ; Humans ; Marijuana Abuse/physiopathology ; Mental Disorders/etiology ; Neuropeptides/physiology ; Recurrence ; Stress, Psychological/complications ; Stress, Psychological/physiopathology ; Substance Withdrawal Syndrome/physiopathology ; Tobacco Use Disorder/physiopathology
Chemical Substances	Neuropeptides ; Corticotropin-Releasing Hormone (9015-71-8)
Language	English
Publishing date	2005-11
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	423722-5
ISSN	1872-6321 ; 0165-0173
ISSN (online)	1872-6321
ISSN	0165-0173
DOI	10.1016/j.brainresrev.2005.01.007
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Zs.A 1506: Show issues

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Article ; Online: Decreased sensitivity to the effects of dopamine D1-like, but not D2-like, receptor antagonism in the posterior hypothalamic region/anterior ventral tegmental area on brain reward function during chronic exposure to nicotine in rats.

Bruijnzeel, Adrie W / Markou, Athina

Brain research

2005 Volume 1058, Issue 1-2, Page(s) 91–100

Abstract: Chronic administration of nicotine induces adaptations in central nervous system function to counteract nicotine's acute effects. When nicotine administration ceases, these adaptations remain unopposed and may lead to drug withdrawal. The present studies ...

Abstract	Chronic administration of nicotine induces adaptations in central nervous system function to counteract nicotine's acute effects. When nicotine administration ceases, these adaptations remain unopposed and may lead to drug withdrawal. The present studies were conducted to assess the effects of chronic nicotine administration on dopamine D1- and D2-like receptor activity in the posterior hypothalamus/anterior ventral tegmental area (VTA). An intracranial self-stimulation discrete trial procedure that provides current intensity thresholds was used to provide a measure of brain reward function in rats. Previous studies showed that systemic administration of dopamine D1- or D2-like receptor antagonists induced elevations in brain reward thresholds in drug-free rats, indicative of a decrease in brain reward function. We show here that injections of the D1-like receptor antagonist SCH 23390 (1-4 microg total bilateral dose) into the posterior hypothalamus/anterior VTA differentially elevated brain reward thresholds in rats chronically treated with nicotine (9 mg/kg/day, salt) versus saline-treated rats. The nicotine-treated rats were less sensitive to the threshold elevating effects of D1-like receptor antagonism. By contrast, the D2-like receptor antagonist eticlopride (1-4 microg total bilateral dose) injected into the posterior hypothalamus/anterior VTA significantly elevated brain reward thresholds in saline- and nicotine-treated rats. No differential effect of eticlopride on brain reward thresholds in saline- and nicotine-treated rats was observed. Decreased sensitivity to D1-like receptor antagonism in the posterior hypothalamus/anterior VTA may partly mediate the development of tolerance to the reinforcing effects of nicotine and the manifestation of negative affective signs associated with cessation of nicotine administration.
MeSH term(s)	Animals ; Disease Models, Animal ; Dopamine D2 Receptor Antagonists ; Drug Administration Schedule ; Drug Tolerance/physiology ; Hypothalamus, Posterior/drug effects ; Hypothalamus, Posterior/metabolism ; Male ; Nicotine/pharmacology ; Nicotinic Agonists/pharmacology ; Rats ; Rats, Wistar ; Receptors, Dopamine D1/antagonists & inhibitors ; Receptors, Dopamine D1/metabolism ; Receptors, Dopamine D2/metabolism ; Reward ; Substance Withdrawal Syndrome/metabolism ; Substance Withdrawal Syndrome/physiopathology ; Tobacco Use Disorder/metabolism ; Tobacco Use Disorder/physiopathology ; Ventral Tegmental Area/drug effects ; Ventral Tegmental Area/metabolism
Chemical Substances	Dopamine D2 Receptor Antagonists ; Nicotinic Agonists ; Receptors, Dopamine D1 ; Receptors, Dopamine D2 ; Nicotine (6M3C89ZY6R)
Language	English
Publishing date	2005-10-05
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1200-2
ISSN	1872-6240 ; 0006-8993
ISSN (online)	1872-6240
ISSN	0006-8993
DOI	10.1016/j.brainres.2005.07.056
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Zs.A 161: Show issues

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Article ; Online: Effects of insulin and leptin in the ventral tegmental area and arcuate hypothalamic nucleus on food intake and brain reward function in female rats.

Bruijnzeel, Adrie W / Corrie, Lu W / Rogers, Jessica A / Yamada, Hidetaka

Behavioural brain research

2011 Volume 219, Issue 2, Page(s) 254–264

Abstract: There is evidence for a role of insulin and leptin in food intake, but the effects of these adiposity signals on the brain reward system are not well understood. Furthermore, the effects of insulin and leptin on food intake in females are ... ...

Abstract	There is evidence for a role of insulin and leptin in food intake, but the effects of these adiposity signals on the brain reward system are not well understood. Furthermore, the effects of insulin and leptin on food intake in females are underinvestigated. These studies investigated the role of insulin and leptin in the ventral tegmental area (VTA) and the arcuate hypothalamic nucleus (Arc) on food intake and brain reward function in female rats. The intracranial self-stimulation procedure was used to assess the effects of insulin and leptin on the reward system. Elevations in brain reward thresholds are indicative of a decrease in brain reward function. The bilateral administration of leptin into the VTA (15-500 ng/side) or Arc (15-150 ng/side) decreased food intake for 72 h. The infusion of leptin into the VTA or Arc resulted in weight loss during the first 48 (VTA) or 24 h (Arc) after the infusions. The administration of insulin (0.005-5 mU/side) into the VTA or Arc decreased food intake for 24 h but did not affect body weights. The bilateral administration of low, but not high, doses of leptin (15 ng/side) or insulin (0.005 mU/side) into the VTA elevated brain reward thresholds. Neither insulin nor leptin in the Arc affected brain reward thresholds. These studies suggest that a small increase in leptin or insulin levels in the VTA leads to a decrease in brain reward function. A relatively large increase in insulin or leptin levels in the VTA or Arc decreases food intake.
MeSH term(s)	Animals ; Arcuate Nucleus of Hypothalamus/physiology ; Brain/physiology ; Conditioning, Operant/drug effects ; Eating/drug effects ; Electrodes, Implanted ; Female ; Hypoglycemic Agents/administration & dosage ; Hypoglycemic Agents/pharmacology ; Insulin/administration & dosage ; Insulin/pharmacology ; Leptin/administration & dosage ; Leptin/pharmacology ; Microinjections ; Rats ; Rats, Sprague-Dawley ; Reward ; Self Stimulation ; Ventral Tegmental Area/physiology
Chemical Substances	Hypoglycemic Agents ; Insulin ; Leptin
Language	English
Publishing date	2011-01-19
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	449927-x
ISSN	1872-7549 ; 0166-4328
ISSN (online)	1872-7549
ISSN	0166-4328
DOI	10.1016/j.bbr.2011.01.020
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Zs.A 1599: Show issues

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Article ; Online: Corticotropin-releasing factor-1 receptor activation mediates nicotine withdrawal-induced deficit in brain reward function and stress-induced relapse.

Bruijnzeel, Adrie W / Prado, Melissa / Isaac, Shani

Biological psychiatry

2009 Volume 66, Issue 2, Page(s) 110–117

Abstract: Background: Tobacco addiction is a chronic brain disorder that is characterized by a negative affective state upon smoking cessation and relapse after periods of abstinence. Previous research has shown that blockade of corticotropin-releasing factor ( ... ...

Abstract	Background: Tobacco addiction is a chronic brain disorder that is characterized by a negative affective state upon smoking cessation and relapse after periods of abstinence. Previous research has shown that blockade of corticotropin-releasing factor (CRF) receptors with a nonspecific CRF1/CRF2 receptor antagonist prevents the deficit in brain reward function associated with nicotine withdrawal and stress-induced reinstatement of extinguished nicotine-seeking in rats. The aim of these studies was to investigate the role of CRF1 and CRF2 receptors in the deficit in brain reward function associated with precipitated nicotine withdrawal and stress-induced reinstatement of nicotine-seeking. Methods: The intracranial self-stimulation (ICSS) procedure was used to assess the negative affective state of nicotine withdrawal. Elevations in brain reward thresholds are indicative of a deficit in brain reward function. Stress-induced reinstatement of nicotine-seeking was investigated in animals in which responding for intravenously infused nicotine was extinguished by substituting saline for nicotine. Results: In the ICSS experiments, the nicotinic receptor antagonist mecamylamine elevated the brain reward thresholds of the nicotine-dependent rats but not those of the control rats. The CRF1 receptor antagonist R278995/CRA0450 but not the CRF2 receptor antagonist astressin-2B prevented the elevations in brain reward thresholds associated with precipitated nicotine withdrawal. Furthermore, R278995/CRA0450 but not astressin-2B prevented stress-induced reinstatement of extinguished nicotine-seeking. Neither R278995/CRA0450 nor astressin-2B affected operant responding for chocolate-flavored food pellets. Conclusions: These studies indicate that CRF(1) receptors but not CRF(2) receptors play an important role in the anhedonic-state associated with acute nicotine withdrawal and stress-induced reinstatement of nicotine-seeking.
MeSH term(s)	Animals ; Benzenesulfonates/pharmacology ; Brain/physiology ; Corticotropin-Releasing Hormone/pharmacology ; Extinction, Psychological/drug effects ; Food ; Injections, Intraventricular ; Male ; Nicotine/adverse effects ; Peptide Fragments/pharmacology ; Psychomotor Performance/drug effects ; Quinolines/pharmacology ; Rats ; Rats, Wistar ; Receptors, Corticotropin-Releasing Hormone/antagonists & inhibitors ; Receptors, Corticotropin-Releasing Hormone/physiology ; Recurrence ; Reward ; Self Stimulation ; Stress, Psychological/physiopathology ; Stress, Psychological/psychology ; Substance Withdrawal Syndrome/physiopathology ; Substance Withdrawal Syndrome/psychology
Chemical Substances	1-(8-(2,4-dichlorophenyl)-2-methylquinolin-4-yl)-1,2,3,6-tetrahydropyridine-4-carboxamide benzenesulfonate ; Benzenesulfonates ; Peptide Fragments ; Quinolines ; Receptors, Corticotropin-Releasing Hormone ; astressin (170809-51-5) ; CRF receptor type 1 (5CLY6W2H1M) ; Nicotine (6M3C89ZY6R) ; Corticotropin-Releasing Hormone (9015-71-8)
Language	English
Publishing date	2009-02-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2009.01.010
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Zs.A 720: Show issues

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Article: Adaptations in cholinergic transmission in the ventral tegmental area associated with the affective signs of nicotine withdrawal in rats.

Bruijnzeel, Adrie W / Markou, Athina

Neuropharmacology

2004 Volume 47, Issue 4, Page(s) 572–579

Abstract: Chronic administration of nicotine induces adaptations in the brain reward circuit to counteract the acute drug effects; when nicotine administration ceases, these adaptations remain unopposed and lead to drug withdrawal. The present studies were ... ...

Abstract	Chronic administration of nicotine induces adaptations in the brain reward circuit to counteract the acute drug effects; when nicotine administration ceases, these adaptations remain unopposed and lead to drug withdrawal. The present studies were conducted to assess the effects of chronic nicotine administration on nicotinic acetylcholine receptor (nAChR) activity in the ventral tegmental area (VTA) and the nucleus accumbens (Nacc) shell. A discrete-trial intracranial self-stimulation procedure that provides current-intensity thresholds as measures of brain reward function was used in rats. Previous studies have shown that withdrawal from nicotine-induced elevations in brain reward thresholds that are indicative of a decrease in brain reward function. We show here that injections of the nAChR antagonist dihydro-beta-erythroidine (DHbetaE; 0.6-20 microg total bilateral dose) into the VTA, but not outside the VTA, resulted in significant elevations in brain reward thresholds in nicotine dependent rats (9 mg/kg/day nicotine hydrogen tartrate) while having no effect in saline-treated controls. By contrast, DHbetaE (0.6-20 microg total bilateral dose) injected into the Nacc shell had no effect on brain reward thresholds of nicotine- or saline-treated rats. The adaptations in cholinergic transmission in the VTA are likely to mediate, at least partly, the affective signs of nicotine withdrawal in humans.
MeSH term(s)	Adaptation, Physiological/drug effects ; Adaptation, Physiological/physiology ; Animals ; Cholinergic Fibers/drug effects ; Cholinergic Fibers/physiology ; Dihydro-beta-Erythroidine/pharmacology ; Dose-Response Relationship, Drug ; Male ; Nicotine/administration & dosage ; Rats ; Rats, Wistar ; Substance Withdrawal Syndrome ; Synaptic Transmission/drug effects ; Synaptic Transmission/physiology ; Ventral Tegmental Area/drug effects ; Ventral Tegmental Area/physiology
Chemical Substances	Dihydro-beta-Erythroidine (23255-54-1) ; Nicotine (6M3C89ZY6R)
Language	English
Publishing date	2004-09
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2004.05.005
Database	MEDical Literature Analysis and Retrieval System OnLINE

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