The effect of intrahippocampal infusion of quinolinic acid (Quin), an endogenous excitatory amino acid, was studied on the amygdala kindling. Quin 120 nmol injected intrahippocampally 2 wk prior to the beginning of amygdala kindling significantly not only produced dorsal hippocampal pyramidal and granule cell loss but also decreased the number of stimuli to trigger the stage 5 seizures of amygdala kindling. In kindled rats, intrahippocampal 20 nmol Quin infusion fully inhibited the stage 5 of amygdala-kindled seizures. The inhibitory effect of Quin was antagonized by dl-2-amino-7-phosphonoheptanoic acid, a selective antagonist of N-methyl-D-aspartate (NMDA) type receptors. The results suggest that NMDA-type receptors in the hippocampus may play a role in the control of the seizure threshold in the amygdala.