Abstract
The influence of audiogenic seizures (AGS) on synaptic facilitation was studied in DBA/2J (D2) and C57BL/6J (B6) mice. AGS susceptibility is inherited in D2 mice, but can be acquired in AGS-resistant B6 mice through acoustic priming. The experiments were performed on hippocampal slices obtained from D2 and B6 mice both with and without seizures. Long-term potentiation (LTP) and low-Mg(2+)-induced synaptic facilitation (LMISF) were evaluated after stimulation of Schaffer collaterals. The magnitude of LTP and LMISF was significantly greater in slices obtained from mice with seizures than from mice without seizures in both strains. Seizure-induced enhancement of LTP and LMISF was markedly reduced by the N-methyl-D-aspartate (NMDA) receptor antagonist AP-5. The noncompetitive NMDA receptor antagonist MK 801 reduced the efficiency of priming in B6 mice and abolished AGS in D2 mice and primed B6 mice. The data suggest that audiogenic seizures can enhance synaptic facilitation through activation of the NMDA receptor.
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