HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 90/4/2785    most recent 00482.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Liu, X. Articles by Misgeld, U. Search for Related Content PubMed PubMed Citation Articles by Liu, X. Articles by Misgeld, U.

Report

KCC2 Mediates NH₄⁺ Uptake in Cultured Rat Brain Neurons

Institut für Physiologie und Pathophysiologie und Interdisziplinäres Zentrum für Neurowissenschaften, Universität Heidelberg, D-69120 Heidelberg, Germany

Submitted 10 May 2003; accepted in final form 3 August 2003

Elevated levels of in the brain impair neuronal function. We studied the effects of on postsynaptic inhibition of cultured rat brain neurons using whole cell recording under nominally -free conditions. Application of shifted the reversal potentials for spontaneous inhibitory postsynaptic currents and currents elicited by dendritic GABA applications in a positive direction because [Cl^–]_i increased. The positive shift of the reversal potentials of GABA-induced Cl^– currents was equal on equimolar elevation of or [K⁺]_o, respectively. The -induced increase in [Cl^–]_i was reversed by an inhibitor of cation-anion cotransport, furosemide (0.1 mM), but not by bumetanide (0.01 mM) or by replacement of [Na⁺]_o by Li⁺. We conclude that neuron-specific K-Cl cotransporter (KCC2) transports similar to K⁺. Despite this fact, the small increase of during metabolic encephalopathies will barely elevate [Cl^–]_i. However, an impairment of neuronal function may result because KCC2 provides a pathway to accumulate , and thereby, a continuous acid load to neurons.

This article has been cited by other articles:

				G. Gamba Molecular Physiology and Pathophysiology of Electroneutral Cation-Chloride Cotransporters Physiol Rev, April 1, 2005; 85(2): 423 - 493. [Abstract] [Full Text] [PDF]

				J. R. Williams and J. A. Payne Cation transport by the neuronal K+-Cl- cotransporter KCC2: thermodynamics and kinetics of alternate transport modes Am J Physiol Cell Physiol, October 1, 2004; 287(4): C919 - C931. [Abstract] [Full Text] [PDF]