Abstract
Publisher Summary Glutamate plays a central role in the neuronal circuitry that recruits neurons into epileptic discharges. Metabotropic glutamate receptors (mGluRs) are the G-protein coupled class of glutamate receptor. The release of glutamate during seizures can kill neurons, mainly as a result of Ca 2+ entering with the Na + and K + through the N-methyl-D-aspartate (NMDA) receptors and certain kinds of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors. In the hippocampal CA3 region, glutamatergic synapses among pyramidal cells provide the substrate for a chain reaction, which leads to the synchronous epileptic discharge. Both AMPA and NMDA receptors are present at these recurrent synapses. AMPA receptors are responsible for the synchronization of epileptic bursts in the bicuculline/picrotoxin models and NMDA in the low-Mg 2+ model. The slower kinetics of NMDA receptors can prolong discharges from the ∼100 ms of the interictal spike to the first few hundred ms of an afterdischarge. Events lasting as long as a full seizure can occur in several experimental epilepsies in the slice.
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