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The Expanding Therapeutic Potential of Neuronal KCC2
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Journal Article
The Expanding Therapeutic Potential of Neuronal KCC2
2020
Overview
Dysfunctions in GABAergic inhibitory neural transmission occur in neuronal injuries and neurological disorders. The potassium–chloride cotransporter 2 (KCC2, SLC12A5) is a key modulator of inhibitory GABAergic inputs in healthy adult neurons, as its chloride (Cl−) extruding activity underlies the hyperpolarizing reversal potential for GABAA receptor Cl− currents (EGABA). Manipulation of KCC2 levels or activity improve symptoms associated with epilepsy and neuropathy. Recent works have now indicated that pharmacological enhancement of KCC2 function could reactivate dormant relay circuits in an injured mouse’s spinal cord, leading to functional recovery and the attenuation of neuronal abnormality and disease phenotype associated with a mouse model of Rett syndrome (RTT). KCC2 interacts with Huntingtin and is downregulated in Huntington’s disease (HD), which contributed to GABAergic excitation and memory deficits in the R6/2 mouse HD model. Here, these recent advances are highlighted, which attest to KCC2’s growing potential as a therapeutic target for neuropathological conditions resulting from dysfunctional inhibitory input.
Publisher
MDPI AG,MDPI
Subject
/ Epilepsy
/ GABAergic Neurons - drug effects
/ GABAergic Neurons - metabolism
/ Humans
/ Huntington Disease - drug therapy
/ Huntington Disease - metabolism
/ Huntington Disease - therapy
/ Injuries
/ Kinases
/ Mice
/ Mutation
/ Pain
/ Potassium-chloride cotransporter
/ Proteins
/ Rett Syndrome - drug therapy
/ Solute Carrier Family 12, Member 2 - metabolism
/ Spinal Cord Injuries - metabolism
