Amygdaloid kindling, in which repeated application of low intensity electrical stimulation to the amygdala at appropriate intervals results in the progressive development of generalized convulsive seizures, is an animal model of complex partial epilepsy. The present article describes data that were recently collected to study the possible roles of excitatory amino acids in the kindling phenomenon. The results suggest an involvement of the amino acids in the enhanced trans-synaptic excitability responsible for the expression and generalization of kindled amygdaloid convulsions.