CHOLECYSTOKININ-OCTAPEPTIDE AND THE D-2 ANTAGONIST RACLOPRIDE INDUCE FOS-LIKE IMMUNOREACTIVITY IN THE SHELL PART OF THE RAT NUCLEUS-ACCUMBENS VIA DIFFERENT MECHANISMS

Induction of neuronal Fos-like immunoreactivity (IR) in the rat brain by cholecystokinin octapeptide (CCK-8) and the dopamine (DA) D-2 recep tor antagonist raclopride was demonstrated. In vivo treatment with the CCK-8 (0.01, 0.1 and 1 nmol/rat, i.c.v.) or the D-2 antagonist raclop ride (0.1, 0.5 and 1 mg/kg, i.p.) alone increased in a dose-dependent way the Fos-like ir profiles in the shell part of the rat nucleus accu mbens (AcbSh). Combined treatment with CCK-8 (0.1 nmol/rat) and raclop ride (0.5 mg/kg) caused significant additive increases in the Fos-like ir profiles in the AcbSh. In the central caudate-putamen, the medial olfactory tubercle, and the frontal cerebral cortex where either compo und alone was weakly active or inactive, the combined treatment with b oth compounds led to a significant induction of neuronal Fos-like ir p rofiles. These results suggest that the blockade of D-2 and activation of CCK transduction lines can induce Fos-like IR via different mechan isms. They may produce additive effects in AcbSh and synergistic effec ts in the caudate-putamen and the olfactory tubercle on the induction of neuronal Fos-like IR and thus on long-term regulation of gene expre ssion in the striatum.