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Nicotine reinforcement is reduced by cannabinoid CB 1 receptor blockade in the ventral tegmental area
Author(s) -
Simonnet Amelie,
Cador Martine,
Caille Stephanie
Publication year - 2013
Publication title -
addiction biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.445
H-Index - 78
eISSN - 1369-1600
pISSN - 1355-6215
DOI - 10.1111/j.1369-1600.2012.00476.x
Subject(s) - nicotine , ventral tegmental area , nucleus accumbens , cannabinoid , cannabinoid receptor , pharmacology , antagonist , self administration , nicotine withdrawal , medicine , chemistry , neuroscience , receptor , psychology , dopamine , dopaminergic
Abstract Cannabinoid type 1 ( CB 1) receptors control the motivational properties and reinforcing effects of nicotine. Indeed, peripheral administration of a CB 1 receptor antagonist dramatically decreases both nicotine taking and seeking. However, the neural substrates through which the cannabinoid CB 1 receptors regulate the voluntary intake of nicotine remain to be elucidated. In the present study, we sought to determine whether central injections of a CB 1 receptor antagonist delivered either into the ventral tegmental area ( VTA ) or the nucleus accumbens ( NAC ) may alter nicotine intravenous self‐administration ( IVSA ). Rats were first trained to self‐administer nicotine (30 μg/kg/0.1 ml). The effect of central infusions of the CB 1 antagonist AM 251 (0, 1 and 10 μg/0.5 μl/side) on nicotine‐taking behavior was then tested. Intra‐ VTA infusions of AM 251 dose dependently reduced IVSA with a significant decrease for the dose 10 μg/0.5 μl/side. Moreover, operant responding for water was unaltered by intra‐ VTA AM 251 at the same dose. Surprisingly, intra‐ NAC delivery of AM 251 did not alter nicotine behavior at all. These data suggest that in rats chronically exposed to nicotine IVSA , the cannabinoid CB 1 receptors located in the VTA rather than in the NAC specifically control nicotine reinforcement and, subsequently, nicotine‐taking behavior.