Altered GABAA receptor subunit expression at thalamocortical synapses in an animal model of absence epilepsy

Abstract

Absence epilepsy is a non-convulsive generalized form of epilepsy, characterized by spike-wave discharges, which predominantly affects children. It is accompanied by sudden impairment of consciousness and has an adverse impact on childhood learning. While disruption of the thalamocortical (TC) network is known to lead to generation of hypersynchronous intrathalamic oscillatory activity during absence seizures, the underlying cellular and molecular mechanisms remain largely unknown. Recent studies using human and animal models suggest region-specific changes in GABAA receptors (GABAAR) in the thalamus may underlie hypersynchronous oscillations in absence seizures.