Effects of morphine on dopamine-stimulated adenylate cyclase and on cyclic GMP formation in primate brain amygdaloid nucleus

In homogenates of Macacamulatta (Rhesus) or Cebusapella amygdaloid nuclear complex, adenylate cyclase activity was approximately doubled by either 10μM dopamine or 8mM NaF. In the presence of morphine, the stimulation by dopamine was reduced. A 90–100% inhibition of the dopamine stimulation was obtained with 20μM, and a 50% inhibition, with 5μM morphine. The effects of 10μM morphine on dopamine stimulation were reversed by 10μM naloxone. Morphine itself did not significantly affect the basal adenylate cyclase activity, but in the presence of 10μM morphine the stimulation by 8mM NaF was reduced approxiamtely 50%. The data suggest an action of morphine at a receptor site which is distinct from the dopamine receptor, but which inhibits the dopamine-stimulated adenylate cyclase. In addition, the cyclic GMP content of Cebus amygdala slices was reduced by 50–75% during incubation for 5–20 minutes with morphine. Maximum effects on cyclic GMP were obtained with 10μM, and half-maximum effects, with 0.1μM morphine. The effect of morphine on amygdala cyclic GMP was not reversed by naloxone. Thus, this action of morphine may not be receptor mediated, or may involve the interaction of morphine with receptors other than the opiate receptor.