PERSISTENCE OF THE RELEASABLE POOL OF CCK IN THE RAT NUCLEUS-ACCUMBENS AND CAUDATE-PUTAMEN FOLLOWING LESIONS OF THE MIDBRAIN

Previous studies have identified populations of dopamine neurons in th e midbrain that colocalize cholecystokinin some of which project to th e nucleus accumbens and caudate-putamen. The contribution of dopamine- colocalized peptide to the total releasable pool of cholecystokinin in these brain regions was investigated using microdialysis. Dopamine, d ihydroxyphenylacetic acid and cholecystokinin immunoreactive levels in dialysates of the posterior medial nucleus accumbens and medial cauda te-putamen were determined following 6-hydroxydopamine lesions of the ventral tegmental area and substantia nigra or transection of the medi al forebrain bundle. An 89-99% depletion in basal extracellular dihydr oxyphenylacetic acid and an 87-99% decrease in veratridine-evoked extr acellular dopamine levels was observed in the nucleus accumbens and ca udate-putamen, 4 weeks after 6-hydroxydopamine lesion. No statisticall y significant difference was observed between lesioned and control ani mals in the basal or veratridine-evoked extracellular level of cholecy stokinin immunoreactivity in either region. Similarly, transection of the medial forebrain bundle failed to significantly deplete the releas able pool of cholecystokinin immunoreactivity in the nucleus accumbens or caudate nucleus despite 89-99% depletions of dopamine and its meta bolite. These data suggest that midbrain dopamine or non-dopaminergic cells are not the primary source of releasable cholecystokinin in the posterior medial nucleus accumbens and medial caudate-putamen measured by microdialysis.