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Cannabinoid-serotonin interactions in alcohol-preferring vs alcohol-avoiding mice

Cannabinoid-serotonin interactions in alcohol-preferring vs alcohol-avoiding mice

  1. Jasim
    Because cannabinoid and serotonin (5-HT) systems have
    been proposed to play an important role in drug craving, we
    investigated whether cannabinoid 1 (CB1) and 5-HT1A
    receptor ligands could affect voluntary alcohol intake in two
    mouse strains, C57BL/6 J and DBA/2 J, with marked differences
    in native alcohol preference. When offered progressively
    (3–10% ethanol) in drinking water, in a free-choice
    procedure, alcohol intake was markedly lower ( 70%) in
    DBA/2 J than in C57BL/6 J mice. In DBA/2 J mice, chronic
    treatment with the cannabinoid receptor agonist WIN 55,212–
    2 increased alcohol intake. WIN 55,212–2 effect was
    prevented by concomitant, chronic CB1 receptor blockade by
    rimonabant or chronic 5-HT1A receptor stimulation by 8-hydroxy-
    2-(di-n-propylamino)-tetralin, which, on their own, did not
    affect alcohol intake. In C57BL/6 J mice, chronic treatment
    with WIN 55,212–2 had no effect but chronic CB1 receptor
    blockade or chronic 5-HT1A receptor stimulation significantly
    decreased alcohol intake. Parallel autoradiographic investigations
    showed that chronic treatment with WIN 55,212–2
    significantly decreased 5-HT1A-mediated [35S]guanosine triphosphate-
    c-S binding in the hippocampus of both mouse
    strains. Conversely, chronic rimonabant increased this binding
    in C57BL/6 J mice. These results show that cannabinoid
    neurotransmission can exert a permissive control on alcohol
    intake, possibly through CB1–5–HT1A interactions. However,
    the differences between C57BL/6 J and DBA/2 J mice indicate
    that such modulations of alcohol intake are under genetic
    control.