Systemic injection of kainic acid: effect on neurotransmitter markers in piriform cortex, amygdaloid complex and hippocampus and protection by cortical lesioning and anticonvulsants.

Systemic injection of kainic acid (12 mg/kg) in rats induces a well established pattern of neuronal lesions in different brain regions. These lesions are accompanied by changes in neurotransmitter markers. In the piriform cortex and amygdaloid complex, the kainic acid lesion was accompanied by a reduction in the high affinity uptake of glutamate and in the activities of glutamate decarboxylase and choline acetyltransferase, whereas in the hippocampus there was a reduction in the high affinity uptake of glutamate and in glutamate decarboxylase activity. Hemidecortication, hemitransection, a caudal knife cut in the cortex, or treatment with diazepam, all protected against the effects of kainic acid in the piriform cortex and amygdaloid complex but not in the hippocampus. Diphenylhydantoin had no effect on the neurotoxicity of kainic acid. The results indicate that the neurotoxic effects of kainic acid in the piriform cortex and amygdala are dependent on an intact cortical structure, probably due to a dependence on specific excitatory circuitry. The neurons involved may be glutamergic/aspartergic.