Continuous cocaine administration enhances mu- but not delta-opioid receptor-mediated inhibition of adenylyl cyclase activity in nucleus accumbens.

Cocaine alters opioid receptor densities in rat brain. To investigate the functional consequences of such opioid receptor changes, adenylyl cyclase activity was measured in rat nucleus accumbens and caudate putamen following continuous cocaine administration (50 mg/kg/day, 7 days). In the nucleus accumbens chronic cocaine led to an increase in both the number of mu-opioid receptors and the maximal inhibition of adenylyl cyclase activity by DAMGO ([D-Ala2,N-methyl-Phe4,Glyol]enkephalin). There was no effect on inhibition of adenylyl cyclase activity by DPDPE ([D-Pen2,D-Pen5]enkephalin). There were no changes in the caudate putamen. Thus, continuous cocaine administration for 7 days results in a selective increase in mu-opioid receptor-mediated effector function in the nucleus accumbens.