The mediodorsal nucleus (MD) of the thalamus has reciprocal projections with the frontal cortex and limbic system, and may be involved in absence seizures. Kainic acid was injected into the left MD of Wistar rats, and behavior and electroencephalography were monitored for 24 hours, then continued intermittently for 8 weeks. The rat brains were then examined histologically. Brain metabolic changes were also investigated by intravenous injection of 100 mCi/kg of [ 14 C]2-deoxyglucose to measure local cerebral glucose metabolism. Bilateral synchronous spike and wave complexes appeared almost 2 hours after kainic acid injection, and the waveforms continued for about 5-7 hours in the bilateral MDs, ipsilateral sensorimotor cortex, and basolateral nucleus of the amygdala. The associated behavioral changes were mainly those of behavioral arrest and staring, associated with occasional limbic seizures. Clear metabolic increases were found in the ipsilateral frontal cortex, hippocampus, and amygdala. The present results suggest that the MD was involved in both the mechanism of spike and wave complexes in the bilateral frontal cortices, and in seizure propagation to the limbic system. Consequently, kainic acid-induced MD seizure is associated with significant cognitive impairment and may explain the mechanism of petit mal seizure.

The inhibitory effects of deep brain stimulation (DBS) were investigated in a rat model of kainic acid (KA)-induced limbic status epilepticus. Wistar rats were injected with 1.0 mg KA into the left amygdala after stereotactic implantation of a guide cannula and electrodes. Bipolar rectangular pulses of 0.1 msec duration and 0.1-0.3 mA amplitude were applied intermittently to the left amygdala (10 Hz or 130 Hz), left ventral hippocampus (10 Hz), and left dorsomedial thalamus (130 Hz). Seizure frequency was evaluated by video electroencephalography monitoring and compared to control animals that did not receive DBS. All rats developed limbic status epilepticus 60-90 minutes after KA injection. Seizure frequency was significantly reduced by 10 Hz stimulation of the amygdala and by 130 Hz stimulation of the dorsomedial thalamus. No significant effects were observed with other types of stimulation. Seizure behaviors or duration of seizure were not changed significantly by DBS treatment. DBS of an epileptic focus may attenuate KA-induced limbic seizures, depending on the stimulation sites and parameters.

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