Star players sidelined in chloride homeostasis in neurons.

Chang-Hoon Cho

doi:10.3389/fncel.2014.00114

Abstract

Star players sidelined in chloride homeostasis in neurons.

Highlights

Edited by: Andrea Barberis, Fondazione Istituto Italiano di Tecnologia, Italy Reviewed by: Yehezkel Ben-Ari, Institut National de la Santé et de la Recherche Médicale, France
Mutations and/or malfunction of Cl−-permeable membrane proteins may disturb chloride homeostasis leading to diverse disease states including hypertension, hepatic encephalopathy, neuropathic pain, and epilepsy (Huberfeld et al, 2007; Price et al, 2009; Li et al, 2012; Ye et al, 2012)
GABA is principally inhibitory, while in immature neurons, GABA can be excitatory. These pleiotropic effects of GABA are believed to be controlled by [Cl−]i, which is developmentally regulated by two cation chloride cotransporters (CCCs), NKCC1, and KCC2, that allow Cl− to move in and out of the cells,respectively (Ben-Ari et al, 2007; Blaesse et al, 2009)

Summary

Introduction

Edited by: Andrea Barberis, Fondazione Istituto Italiano di Tecnologia, Italy Reviewed by: Yehezkel Ben-Ari, Institut National de la Santé et de la Recherche Médicale, France. Local impermeant anions establish the neuronal chloride concentration by Glykys, J., Dzhala, V., Egawa, K., Balena, T., Saponjian, Y., Kuchibhotla, K. The chloride ion (Cl−) is the most abundant physiological anion and is involved in many cellular functions including intracellular membrane trafficking, volume control, and excitability, as well regulating short- and long-term plasticity in neurons (Woodin et al, 2003; De Koninck, 2007; Raimondo et al, 2012; Succol et al, 2012; Stauber and Jentsch, 2013).

Results

Conclusion