Morphine or norepinephrine at 10 p~ inhibit adenylate cyclase of NG108-15 neuroblastoma x glioma hybrid cells and gradually, over a period of 12 h or more, elicit a compensatory, persistent increase in adenylate cyclase activity. The cells are then dependent upon the receptor ligand for maintenance of normal cyclic AMP levels. Serum lipids or linoleic acid are required for the full expression of the long-lived morphine-dependent increase in adenylate cyclase activity, but serum lipids are not required for inhibition of the enzyme by morphine. Serum lipids are also not required for the full expression of the norepinephrine-dependent increase in adenylate cyclase activity. In the NG108-15 model system, therefore, the acquisition of dependence upon morphine can be dissociated from the inhibition of adenylate cyclase by morphine as well as from the acquisition of dependence upon another receptor ligand, norepinephrine.

No abstract