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Injection of the Neuropeptide CNP into Dopaminergic Rat Brain Areas Decreases Alcohol Intake
Author(s) -
Romieu Pascal,
Gobaille Serge,
Aunis Dominique,
Zwiller Jean
Publication year - 2008
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1432.050
Subject(s) - dopaminergic , ventral tegmental area , endocrinology , neuropeptide , medicine , craving , alcohol , ethanol , chemistry , prefrontal cortex , neuroscience , dopamine , psychology , receptor , addiction , biochemistry , cognition
Alcohol administration is known to alter several brain functions and behaviors in humans and in laboratory animals. One of the targets of ethanol is the mesocorticolimbic dopaminergic reward pathway. We used the “alcohol deprivation effect” test as a rat model of alcohol craving and relapse. The effect is characterized by increased alcohol intake and preference after several weeks of voluntary alcohol consumption followed by a withdrawal phase. The alcohol deprivation effect was found to be considerably reduced by the injection in dopaminergic brain structures of the neuropeptide CNP. This peptide is the most abundant natriuretic peptide in the brain, and signals via an intracellular rise in cyclic GMP. The effect of CNP was observed whether the peptide was injected in situ into the ventral tegmental area or into the prefrontal cortex. It was partially reversed by the injection in the same structures of KT5823, a selective inhibitor of the cGMP‐dependent protein kinase. The results indicate that changes of cyclic GMP levels in dopaminergic rat brain areas participate in the neurobiological mechanisms underlying alcohol craving after withdrawal and/or alcohol dependence.