Dopaminergic mediation of beta-endorphin-induced catalepsy.

Acute intracisternal administration of human beta-endorphin produced catalepsy and increased striatal concentrations of 3,4-dihydroxyphenylacetic acid (DOPA) and homovanillic acid (HVA). All of these effects were blocked by naloxone. Apomorphine, a dopamine receptor antagonist, also prevented beta-endorphin-induced catalepsy and the increase in striatal DOPAC and HVA. The combination of subcataleptic doses of haloperidol and beta-endorphin produced catalepsy and large increases in striatal DOPAC and HVA. These data provide evidence for a role for nigrostriatal dopamine neurons in beta-endorphin-induced catalepsy. The apparent increase in striatal dopamine turnover following beta-endorphin administration may be compensatory.