Blocking of morphine-induced locomotor hyperactivity by amygdaloid lesions in C57BL/6 mice

Bilateral lesions of the amygdaloid complex in C57BL/6 mice prevented the occurrence of morphine-induced hypermotility (running fit). This effect, that was different from that observed after hippocampal lesions but similar to that observed after caudate lesions, confirms the role of the basal ganglia catecholaminergic system in the development of the motor stimulation consecutive to the administration of this opiate receptor agonist.