Induction of delayed synchronized bursts in hippocampal slices by weak sine-wave stimulation; role of the NMDA receptor.

Weak (20-50 microA) sine-wave stimulation at 60 Hz (SWS) of either the mossy fibers or the Schaffer collaterals promoted epileptiform synchronized bursts in the CA2/3 area of rat hippocampal slices in the absence of epileptogenic agents. Following brief SWSs (2-10 sec every 5 min), delayed synchronized bursts (DSBs) were triggered by weak test pulses in either pathway and transmitted to CA1. The long (2-10 sec) refractory periods which followed synchronized bursts in CA2/3 limited their rate of occurrence. Furthermore, SWS decreased the activity for several minutes in slices that exhibited frequent bursts. DSBs were reversibly blocked by perfusion with the N-methyl-D-aspartate (NMDA) specific antagonist DL-2-amino-5-phosphono-valeric acid (APV). The involvement of NMDA receptors was further suggested by the facilitation of CA2/3 synchronized bursts in medium with NMDA (5 microM) or lacking magnesium, and by iontophoresis of NMDA in the CA2/3 stratum radiatum. The findings that SWS-induced DSBs persisted for hours in undisturbed slices, and that bursts abolished by APV reappeared during washout in control solution, suggest long-term changes in the CA2/3 synaptic region.