Calcium modulation of the N-methyl-D-aspartate (NMDA) response and electrographic seizures in immature hippocampus.

Recordings from the CA3 region of hippocampal slices indicate a developmental change in the divalent cation sensitivity of the response elicited by N-methyl-D-aspartate (NMDA) application. In parallel experiments a developmental difference is demonstrated in the capacity of extracellular calcium to modulate electrographic seizure generation. Calcium modulation of the NMDA-elicited response may contribute to the pronounced capacity of immature hippocampus to generate electrographic seizures. Under these conditions activity dependent changes in extracellular calcium could have a greater influence on ion flow produced by activation of the NMDA receptor. The possibility that changes in the receptor isoform may occur during development would have widespread implications for normal cognitive functions and dysfunctions during brain maturation.