Abstract

Induction of neuronal Fos-like immunoreactivity (IR) in the rat brain by cholecystokinin octapeptide (CCK-8) and the dopamine (DA) D 2 receptor 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 raclopride (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 accumbens (AcbSh). Combined treatment with CCK-8 (0.1 nmol/rat) and raclopride (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 compound alone was weakly active or inactive, the combined treatment with both compounds led to a significant induction of neuronal Fos-like ir profiles. These results suggest that the blockade of D 2 and activation of CCK transduction lines can induce Fos-like IR via different mechanisms. They may produce additive effects in AcbSh and synergistic effects in the caudate-putamen and the olfactory tubercle on the induction of neuronal Fos-like IR and thus on long-term regulation of gene expression in the striatum.

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