NDLI: Blockade of CRF1 receptors in the central nucleus of the amygdala attenuates the dysphoria associated with nicotine withdrawal in rats.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Bruijnzeel, Adrie W. Ford, Jenna Rogers, Jessica A. Scheick, Stacey Ji, Yue Bishnoi, Mahendra Alexander, Jon C.
Description	Country affiliation: United States Author Affiliation: Bruijnzeel AW ( Department of Psychiatry, McKnight Brain Institute, University of Florida, 100 S. Newell Dr., Gainesville, Florida 32610, USA. awbruijn@ufl.edu)
Abstract	The majority of smokers relapse during the acute withdrawal phase when withdrawal symptoms are most severe. The goal of the present studies was to investigate the role of corticotropin-releasing factor (CRF) and noradrenergic transmission in the central nucleus of the amygdala (CeA) in the dysphoria associated with smoking cessation. It was investigated if blockade of CRF1 receptors, blockade of 1-adrenergic receptors, or stimulation of 2-adrenergic receptors in the CeA diminishes the deficit in brain reward function associated with nicotine withdrawal in rats. Nicotine dependence was induced by implanting minipumps that delivered a nicotine solution. Withdrawal was precipitated with the nicotinic acetylcholine receptor antagonist mecamylamine. A discrete-trial intracranial self-stimulation procedure was used to assess the negative affective aspects of nicotine withdrawal. Elevations in brain reward thresholds are indicative of a deficit in brain reward function. In all the experiments, mecamylamine elevated the brain reward thresholds of the rats chronically treated with nicotine and did not affect the brain reward thresholds of the saline-treated control rats. Intra-CeA administration of the CRF1 receptor antagonist R278995/CRA0450 completely prevented the mecamylamine-induced elevations in brain reward thresholds in the nicotine-treated rats and did not affect the brain reward thresholds of the saline-treated control rats. R278995/CRA0450 has also been shown to block sigma-1 receptors but there is no evidence that this could affect negative mood states. Intra-CeA administration of the 1-adrenergic receptor antagonist prazosin or the 2-adrenergic receptor agonist clonidine did not affect the brain reward thresholds of the nicotine or saline-treated rats. These studies suggest that CRF1 receptor antagonists may diminish the dysphoria associated with smoking cessation by blocking CRF1 receptors in the CeA.
File Format	HTM / HTML
ISSN	00913057
e-ISSN	18735177
DOI	10.1016/j.pbb.2011.12.001
Journal	Pharmacology Biochemistry and Behavior
Issue Number	1
Volume Number	101
Language	English
Publisher	Elsevier
Publisher Date	2012-03-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Behavioral Sciences Discipline Biochemistry Discipline Pharmacology Amygdala Drug Effects Nicotine Pharmacology Nicotinic Agonists Receptors, Corticotropin-releasing Hormone Antagonists & Inhibitors Smoking Cessation Psychology Substance Withdrawal Syndrome Tobacco Use Disorder Adrenergic Alpha-1 Receptor Antagonists Adrenergic Alpha-2 Receptor Antagonists Animals Benzenesulfonates Clonidine Electrodes, Implanted Mecamylamine Nicotinic Antagonists Prazosin Quinolines Rats, Wistar Drug Therapy Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Biological Psychiatry Behavioral Neuroscience Biochemistry Clinical Biochemistry Toxicology Pharmacology

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