Brain areas involved in production of morphine-induced locomotor hyperactivity of the C57B1/6J mouse.

Previous studies reveal a dose-dependent increase in locomotor activity of the C57B1/6J mouse after administration of morphine or amphetamine. Concurrent partial lesions of both the dorsomedial caudate and lateral septal nuclei resulted in a significant decrease in morphine-induced, but not amphetamine-induced, hyperactivity. Concurrent partial lesions of the nucleus accumbens and stria terminalis produced only a nonsignificant decrease in the morphine-induced hyperactivity. Lesions of the individual brain structures did not significantly affect the morphine-induced locomotor hyperactivity. Microinjections of the opiate antagonist naloxone into discrete portions of the caudate and septal nuclei produced suppression of the morphine-induced hyperactivity response without affecting the hyperactivity caused by amphetamine injections. Only a slight suppression of morphine-induced locomotion was produced when naloxone was injected into the nucleus accumbens and stria terminalis. These data suggest that portions of the caudate and septum may be involved in the mediation of morphine-induced hyperactivity in the C57B1/6J mouse.