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Mol Neurobiol. 2016 May;53(4):2141-51. doi: 10.1007/s12035-015-9162-x. Epub 2015 May 5.

The K(+)-Cl(-) Cotransporter KCC2 and Chloride Homeostasis: Potential Therapeutic Target in Acute Central Nervous System Injury.

Author information

1
Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, 88 Jiefang Road, Hangzhou, 310009, Zhejiang, China.
2
Department of Cardiology, Zhejiang Provincial People's Hospital, Hangzhou, China.
3
Department of Emergency Medicine, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
4
Department of Neurosurgery, New York-Presbyterian Hospital, New York, NY, USA.
5
Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, 88 Jiefang Road, Hangzhou, 310009, Zhejiang, China. hy0904@live.cn.

Abstract

The K(+)-Cl(-) cotransporter-2 (KCC2) is a well-known member of the electroneutral cation-chloride cotransporters with a restricted expression pattern to neurons. This transmembrane protein mediates the efflux of Cl(-) out of neurons and exerts a critical role in inhibitory γ-aminobutyric acidergic (GABAergic) and glycinergic neurotransmission. Moreover, KCC2 participates in the regulation of various physiological processes of neurons, including cell migration, dendritic outgrowth, spine morphology, and dendritic synaptogenesis. It is important to note that down-regulation of KCC2 is associated with the pathogenesis of multiple neurological diseases, which is of particular relevance to acute central nervous system (CNS) injury. In this review, we aim to survey the pathogenic significance of KCC2 down-regulation under the condition of acute CNS injuries. We propose that further elucidation of the molecular mechanisms regarding KCC2 down-regulation after acute CNS injuries is necessary because of potential promising avenues for prevention and treatment of acute CNS injury.

KEYWORDS:

Acute CNS injury; Chloride homeostasis; Excitability; KCC2; Neuron

PMID:
25941074
DOI:
10.1007/s12035-015-9162-x
[Indexed for MEDLINE]

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