Our recent studies on seizure-triggering mechanisms in the kindling model of epilepsy are reviewed. Electroencephalographic (EEG) events during kindling-inducing tetanic stimulation from the site of stimulation were recorded, with an emphasis on EEG suppression and rhythmic synchronous discharge. From electrophysiological and pharmacological analyses of these events, it is hypothesized that activation and subsequent collapse of GABA-A-mediated inhibition is an essential precondition in the initiation of kindled seizures. The excitatory role of NMDA receptors in kindling were also investigated by examining the effects of a noncompetitive antagonist of NMDA receptors (MK-801) on amygdala kindling and hippocampal long-term potentiation (LTP). The results indicate that activation of NMDA receptor complex combined with the collapse of GABA-A-mediated inhibition may be critical for kindling development.