Abstracts

High-frequency electrical stimulation (HFS) suppressed the neuronal activity of the subthalamus (STN), and HFS-STN is effective to control epilepsy. Chemical suppression of STN also suppressed seizures. We have reported that both electrical and chemical suppression of unilateral STN reduced focal neocortical seizures in rats. To clarify the antiepileptic mechanism of STN suppression, we studied changes in cerebral glucose metabolism and benzodiazepine-receptor binding after chemical suppression of STN. A guide cannula was stereotactically implanted into the left sensorimotor cortex and STN of male Wistar rats. Focal cortical seizures were induced by an injection of kainic acid into the left sensorimotor cortex. Using this focal seizure model, 200 ng of muscimol was injected into the left (focus side) STN during seizure status. Sixty minutes later of the muscimol injection, 14C-deoxyglucose was intravenously injected, and local cerebral glucose metabolism was measured with the autoradiographic technique. Change in benzodiazepine-receptor binding was also studied by 125I-iomazenil autoradiography. The data was compared with control group and analyzed statistically. An intracortical injection of kainic acid was induced focal and secondarily generalized seizures in all animals. When the unilateral STN was suppressed by the muscimol injection, seizure status was terminated. Local glucose metabolism was increased in the superior colliculus and interpeduncular nucleus compared with control. The benzodiazepine-receptor binding tended to increase in the ipsilateral cerebral cortex. Chemical suppression of STN lead to hypermetabolism in the superior colliculus, which supported that antilepileptic mechanism of HFS-STN may be activation of the dorsal midbrain region. Furthermore, increase in benzodiazepine-receptor binding of the ipsilateral cerebral cortex is an important result to consider the mechanism of HFS-STN.