The kainic acid model of human temporal lobe epilepsy: The superiority of intra-amygdaloid injection versus other application routes

Abstract

To evaluate the significance of the kainic acid (KA)-induced seizure/brain damage syndrome as an animal model for temporal lobe epilepsy, we compared behavioural and histopathological consequences of intra-amygdaloid (Lam.), intracerebroventricular (Lc.v.) and systemic application of the toxin. I.am. injection of 5 ng KA in conscious freely moving rats via chronically implanted guide cannulas resulted in typical limbic motor seizures in 6 out of 16 rats. Seizures were of short duration, and all rats appeared normal one hour after the injection. Seizure response increased to 70% responding animals with the KA dose raised to 8-15 ng; at this dose range, some animals developed status epilepticus, resulting in neuronal damage in hippocampal CAl and CA 3 sector; in rats undergoing only transient seizure attacks, no brain damage could be detected. I.