Abstract
Tobacco smoking is a well-known risk factor for subsequent alcohol abuse, but the neural events underlying this risk remain largely unknown. Alcohol and nicotine reinforcement involve common neural circuitry, including the mesolimbic dopamine system. We demonstrate in rodents that pre-exposure to nicotine increases alcohol self-administration and decreases alcohol-induced dopamine responses. The blunted dopamine response was due to increased inhibitory synaptic transmission onto dopamine neurons. Blocking stress hormone receptors prior to nicotine exposure prevented all interactions with alcohol that we measured, including the increased inhibition onto dopamine neurons, the decreased dopamine responses, and the increased alcohol self-administration. These results indicate that nicotine recruits neuroendocrine systems to influence neurotransmission and behavior associated with alcohol reinforcement.
Copyright © 2013 Elsevier Inc. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Animals, Newborn
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Central Nervous System Depressants / administration & dosage
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Conditioning, Operant / drug effects
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Dopamine / metabolism*
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Drug Interactions
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Ethanol / administration & dosage
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GABA Antagonists / pharmacology
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Hormone Antagonists / pharmacology
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Hormones / metabolism*
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In Vitro Techniques
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Mifepristone / pharmacology
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Nicotine / pharmacology*
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Nicotinic Agonists / pharmacology*
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Nicotinic Antagonists / pharmacology
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Rats
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Rats, Long-Evans
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Receptors, Nicotinic / metabolism
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Self Administration
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Signal Transduction / drug effects*
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Time Factors
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Tyrosine 3-Monooxygenase / metabolism
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Ventral Tegmental Area / drug effects*
Substances
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Central Nervous System Depressants
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GABA Antagonists
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Hormone Antagonists
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Hormones
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Nicotinic Agonists
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Nicotinic Antagonists
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Receptors, Nicotinic
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nicotinic receptor beta2
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Mifepristone
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Ethanol
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Nicotine
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Tyrosine 3-Monooxygenase
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Dopamine