A MONOCLONAL ANTIIDIOTYPIC ANTIBODY TO OPIOID RECEPTORS LABELS DESIPRAMINE-INDUCED OPIOID BINDING-SITES ON RAT C6 GLIOMA-CELLS AND ATTENUATES THYMIDINE INCORPORATION INTO DNA

Treatment of rat C6 glioma cells with the tricyclic antidepressant des ipramine induces opioid binding. Here the distribution of these opioid -binding sites on C6 cell membranes and a functional property were inv estigated. Immunohistochemical examination of C6 cells was performed u sing a monoclonal anti-idiotypic antibody to opioid receptors (Ab2AOR) . Ab2AOR uniformly labeled >97% of the cells exposed to desipramine ov er their entire surface. The opioid-receptor antagonist naltrexone com pletely blocked Ab2AOR binding. Ab2AOR, which has opioid agonist prope rties, also inhibited DNA synthesis in desipramine-treated but not in naive C6 cells. Similarly, morphine blocked C6 cell proliferation only after desipramine treatment. The antineurotrophic action of Ab2AOR wa s reversed by naltrexone and was insensitive to pertussis toxin. These findings demonstrate that Ab2AOR suppresses the proliferation of C6 g lioma cells by binding to desipramine-induced opioid receptors. (C) 19 94 Wiley-Liss, Inc.