Cholecystokinin potentiation of dopamine-mediated behaviors in the nucleus accumbens

CCK potentiated dopamine- and apomorphine-mediated locomotor and stereotypic behaviors in the nucleus accumbens, but had no effect in the caudate nucleus. The distribution of active sites for behavioral effects parallels the anatomical distribution of co-existing CCK-DA terminal regions. The specificity of CCK in potentiating DA-induced behaviors in the nucleus accumbens, but not in the caudate nucleus, is consistent with the hypothesis that the potentiation phenomenon may be related to the synaptic organization of a co-existing peptide and catecholamine. Possible mechanisms of interaction include modulation at the level of interacting release sites, and, interacting postsynaptic receptor subunits. The CCK-DA co-existence in the mesolimbic pathway of the rat may provide a prototypic model system for delineating the mechanisms by which a neuropeptide modulates a neurotransmitter.