Synaptic Potentiation and Inhibition After Partial Seizures

Seizures induce potentiation of glutamatergic transmission and alteration of inhibitory transmission. Seizure-induced potentiation of glutamatergic transmission is typically found after a single or repeated after-discharges (kindling), but may not be critical for kindling-induced increase in seizure duration and spontaneous interictal spikes. Kindling and status epilepticus induce long-lasting changes of a multi-synaptic circuit involving the entorhinal cortex and hippocampus, but inhibitory changes are different for the dentate gyrus versus CA1. Long-term potentiation is suppressed postictally and interictally in chronic models of partial epilepsy, suggesting that regulation of synaptic plasticity is altered by seizures.