title: Retraction. Clc-2 knockout attenuated experimental temporal lobe epilepsy in mice by tonic inhibition mediated by GABAA receptors.
abstract: Temporal lobe epilepsy (TLE), the most prevalent form of epilepsy, is often associated with drug-resistant seizures. In TLE, altered function of γ-aminobutyric acid (GABA)A receptors (GABAARs) results in potentiation of excitatory and/or failure of inhibitory neurotransmission, which contributes to seizure induction and propagation. Our previous study suggested that chloride channel-2 (Clc-2) contributed to chronically elevated tonic inhibition mediated by GABAARs in a rat model of TLE. In the present study, we used Clc-2 knockout mice to investigate further the role of Clc-2 and its interaction with tonic GABAergic inhibition in a model of TLE. The results revealed that knockout of Clc-2 decreased tonic seizure protection, latency of clonic seizure, seizure threshold and mortality protection in mice. Clc-2 knockout decreased the action potential (AP)peak and APthreshold, Clc-2 currents and GABAAR-mediated tonic inhibition in CA1 pyramidal neurons. Thus, the voltage-gated chloride channel Clc-2, which was functionally upregulated in CA1 pyramidal cells after seizures, may provide protection against TLE by its regulation of action potentials, Clc-2 currents and GABAARs in the CA1 region of the hippocampus.
authors.affiliation: Department of Neurology, Tongji University Affiliated Tenth People's Hospital, Shanghai 200072, PR China. Electronic address: yuxing_ge@yeah.net.
authors.forename: Yu-Xing
authors.initials: YX
authors.lastname: Ge
authors.affiliation: Department of Neurology, Tongji University Affiliated Tenth People's Hospital, Shanghai 200072, PR China.
authors.forename: Xiang-Zhu
authors.initials: XZ
authors.lastname: Tian
keywords: Chloride channel-2; GABA(A) receptors; Temporal lobe epilepsy; Tonic inhibition