Abstract
Gamma-aminobutyric acid type A receptors (GABARs) mediate the majority of brain inhibition and alterations in GABARs are linked to recurrent seizures. Animal models of epilepsy demonstrate altered phasic and tonic inhibition that derives from a change in GABAR number, subunit composition, trafficking, and posttranslational modification. In particular, mutations in δ and γ decrease, while over expression of α6 increase, tonic inhibition. Phasic inhibition is altered via reduction in α1, increases in α4 and loss of δ, either transcriptionally or posttranslationally, leading to synaptic assembly of γ2/α4 containing receptors instead of γ2/α1. In addition, decreased phosphorylation of β3 promotes endocytosis of synaptic GABARs, adding to the diversity of inhibitory changes that may contribute to epileptogenesis.
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