PLASTICITY | Synaptic Potentiation and Inhibition after Partial Seizures

摘要: Seizures may induce long-lasting neural plasticity in the brain that subsequently alter seizure susceptibility and behavioral functions. Potentiation of glutamatergic transmission alteration inhibitory are induced by seizures. Seizure-induced potentiation (SIP) is typically found after a single afterdischarge (AD) or repeated ADs kindling model epilepsy, status epilepticus (SE). However, SIP appears not to be critical for kindling-induced epileptic activities, including increase AD duration and/or severity induction spontaneous interictal spikes. Kindling SE changes multisynaptic circuit involving entorhinal cortex hippocampus, but different somatic versus dendritic synapses dentate gyrus CA1. Regulation synaptic plasticity, ‘metaplasticity,’ altered partial Long-term (LTP) suppressed postictally interictally chronic models epilepsy. LTP (in CA1) theta-frequency primed bursts also hippocampal kindled animals than control animals. We hypothesize decreases efficacy presynaptic inhibition mediated GABAB receptors on GABAergic presyanptic terminals.