Cerebral free amino acids in the amygdaloid kindling model of epilepsy.

A permanent reduction in seizure threshold due to repeated subconvulsive electrical stimulation of the amygdala characterizes the kindling model of epilepsy. Since kindling may involve neurochemical alterations, cerebral amino acids were studied in this induced seizure state. Minimal changes were found in the levels of amino acids in the cerebellum, frontal cortex and brain stem of amygdaloid kindled rats when measured one week after the last seizure. The uptake of taurine into synaptosomes prepared from the cerebellum of kindled rats was significantly elevated, suggesting that alterations in synaptic action of this inhibitory neurotransmitter may play a role in the development of kindling.