Effects of the dihydropyridine Ca²⁺ channel antagonist nimodipine on kainic acid-induced limbic seizures

The effects of the dihydropyridine Ca²⁺ channel antagonist nimodipine on kainic acid-induced seizures were studied in 30 0.5% halothane anesthetized Sprague-Dawley rats. Each animal received low dose kainic acid 0.5 mg/kg i.v. to allow study of the progression of neuronal excitability and epileptiform activity. Preadministration of nimodipine 1.0 mg/kg i.p. increased the latency but did not prevent kainic acid-induced epileptic activity. For example, the latency from kainic acid administration to the appearance of the first seizure and status epilepticus was 75.6 ± 9.1 min and 85.9 ± 9.4 min in control vs. 117.3 ± 9.3 min and 128.0 ± 8.7 min in the nimodipine group (P < 0.005). It is hypothesized that nimodipine attenuated excitability by blocking Ca²⁺ influx through voltage-dependent L-channel secondary to kainic acid-induced membrane depolarization.