Neurofunctional changes in rats in the chronic stage of focal cerebral ischemia induced by left middle cerebral artery (MCA) occlusion were examined. Neurological disorders and behavioral changes were observed with or without methamphetamine administration. Metabolic changes in the basal ganglia following methamphetamine intraperitoneal injection were evaluated by [
14C]deoxyglucose autoradiography 30 days after occlusion. Neurological examination revealed persistent spontaneous rotation to the lesioned side in two of 18 rats, and forelimb flexion to the lesioned side in nine of 18 rats during a 28-day observation period after occlusion. Intraperitoneal administration of methamphetamine (4 mg/kg) induced full 360° rotation toward the lesion side in 14 of 17 rats. The number of rotations was inversely correlated with the size of the intact striatum on the lesion side, especially in rats with cerebral infarct located only in the striatum. Rats with extensive cortical lesion in addition to striatal lesion did not demonstrate this relationship. Deoxyglucose autoradiography in methamphetamine-untreated rats showed symmetrical local cerebral glucose utilization in the basal ganglia except for the subthalamic nucleus, striatum and sensorimotor cortex. Autoradiography in methamphetamine-treated and MCA-occluded rats showed a remarkable increase in glucose utilization in the anterior striatum, entopeduncular nucleus, substantia nigra pars reticulata, and sensorimotor cortex contralateral to the occlusion side, but not on the lesioned side. Rotational movements observed in methamphetamine-treated rats are related to lack of stimulation of the basal ganglia system on the ischemic side. The methamphetamine test may be useful for quantifying masked neuronal dysfunction in the chronic stage of experimental focal cerebral infarct in rats.
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