NMDA receptor blockade inhibits glutamate-induced kindling of the rat amygdala.

Full limbic seizures were kindled in rats by repeated, bi-daily microinjections of glutamate (1.5 mumol) into the basolateral amygdala. Co-administration of the N-methyl-D-aspartate (NMDA) receptor antagonist 2-amino-7-phosphonoheptanoic acid with the glutamate, prevented the development of both electroencephalographic and motor signs of the kindling response. These results indicate an important functional role for NMDA receptors in the development of excitatory amino acid-induced kindling.