Journal
EPILEPSIA
Volume 41, Issue -, Pages S100-S103Publisher
WILEY
DOI: 10.1111/j.1528-1157.2000.tb01566.x
Keywords
hippocampus; NMDA; AMPA; kainate; temporal lobe epilepsy
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Funding
- NINDS NIH HHS [NS-36142] Funding Source: Medline
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Purpose: The contribution of alpha-amino-3-hpdroxy-5-methyl-9-isoxazolepropionic acid (AMPA), N-methyl-D-aspartate (NMDA), and kainate receptor activation to the enhanced seizure susceptibility of the dentate gyrus was investigated in an experimental model of temporal lobe epilepsy. Methods: Using the specific NMDA and AMPA receptor antagonists D-APV and SYM 2206, we examined alterations in glutamate receptor-dependent synaptic currents 48 hours and 25 days after kindling in field-potential and voltage clamp recordings. Results: Forty-eight hours after kindling, the fractions of AMPA and NMDA receptor-mediated excitatory postsynaptic current components shifted dramatically in favor of the NMDA receptor-mediated response. Four weeks after kindling, however, AMPA and NMDA receptor-mediated excitatory postsynaptic currents reverted to control-like values. Neither single nor repetitive perforant path stimuli evoked kainate receptor-mediated excitatory postsynaptic currents in dentate gyrus granule cells of control or kindled rats. Conclusion: The enhanced excitability of the kindled dentate gyrus 48 hours after the last seizure most likely results from transiently enhanced NMDA receptor activation. The NMDA receptor seems to play a critical role in the induction of the kindled state rather than in the persistence of the enhanced seizure susceptibility.
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