Abstract
We examined the effect of electrical stimulation and lesioning of the anterior nucleus of the thalamus (ANT) on focal limbic seizures induced by intraamygdaloid kainic acid (KA) injection in a rat model. To address the mechanism underlying these anti-convulsant actions, cerebral glucose metabolism following ANT electrical stimulation and lesioning was also assessed. Wistar rats were divided into five major groups: control, unilateral and bilateral ANT electrical stimulation, and unilateral and bilateral ANT lesioning. After KA injection, average clinical-seizure frequencies in each group were measured. Local cerebral glucose utilization (LCGU) was also measured using [(14)C] 2-deoxyglucose autoradiography in three groups: control, ANT electrical stimulation and ANT lesioning. Animals subjected to ANT electrical stimulation and lesioning exhibited significantly decreased mean seizure frequency and secondary generalized seizure frequency, compared with control-animals. In control-group, LCGU was markedly increased at both the limbic and corticothalamic circuits sites. While in ANT stimulation or lesioning-group, there was significant reduction in LCGU at the corticothalamic circuit sites, but not so considerable decrease at the limbic structures. ANT electrical stimulation and lesioning in the focal limbic seizure model were effective on convulsive seizures and secondary generalization, specifically with respect to the severity of these seizures.
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