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 controls vs. 117.3 +/- 9.3 min and 128.0 +/- 8.7 min in the nimodipine group (P less than 0.005). It is hypothesized that nimodipine attenuated excitability by blocking Ca2+ influx through voltage-dependent L-channels secondary to kainic acid-induced membrane depolarization.
Paczynski
R P
RP
Department of Neurosurgery, Mayo Clinic, Rochester, MN 55905.
Meyer
F B
FB
Anderson
R E
RE
D000818:Animals; D002118:Calcium / Q000378:metabolism / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D007608:Kainic Acid; D008032:Limbic System / Q000187:drug effects / Q000503:physiopathology*; D009553:Nimodipine / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D012640:Seizures / Q000139:chemically induced* / Q000378:metabolism / Q000503:physiopathology
D002121:Calcium Channel Blockers; D009553:Nimodipine; D007608:Kainic Acid; D002118:Calcium