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Updated: Feb 24, 2026

Study of the Functions and Activities of Neuronal K-Cl Co-Transporter KCC2 Using Western Blotting
Published on: December 9, 2022
Seizing Control of KCC2: A New Therapeutic Target for Epilepsy
Yvonne E Moore1, Matt R Kelley2, Nicholas J Brandon3
1Department of Neuroscience, Physiology and Pharmacology, University College London, London WC1E 6BT, UK; Department of Neuroscience, Tufts University School of Medicine, Boston, MA 02111, USA.
Abstract:
Deficits in GABAergic inhibition result in the abnormal neuronal activation and synchronization that underlies seizures. However, the molecular mechanisms responsible for transforming a normal brain into an epileptic one remain largely unknown. Hyperpolarizing inhibition mediated by type A GABA (GABAA) receptors is dependent on chloride extrusion by the neuron-specific type 2K+-Cl- cotransporter (KCC2). Loss-of-function mutations in KCC2 are a known cause of infantile epilepsy in humans and KCC2 dysfunction is present in patients with both idiopathic and acquired epilepsy. Here we discuss the growing evidence that KCC2 dysfunction has a central role in the development and severity of the epilepsies.
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