Medical amygdala-induced spike potentiation in the rat dentate gyrus is dependent on N-methyl-D-aspartate receptors and subcortical afferents.

We have previously found that high-frequency stimulation of the medial amygdala (MeA) produces a long-lasting potentiation of the population spike at medial perforant path-granule cell synapses in the dentate gyrus of anesthetized rats. The present study was performed to determine whether this novel form of potentiation requires activation of N-methyl-D-aspartate (NMDA) receptors and subcortical afferents. The MeA-induced spike potentiation was completely blocked by the NMDA receptor antagonist 3-((R,S)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (3.5 mg/kg, i.p). When the fimbria-fornix, a major pathway of subcortical afferents, was lesioned, the early phase of MeA-induced spike potentiation remained intact, but the late phase of potentiation was abolished. These results suggest that the NMDA receptor is essentially required for the induction of MeA-induced spike potentiation, while subcortical afferents contribute to the establishment of potentiation.