KCC2 mediates NH4+ uptake in cultured rat brain neurons

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 current...

Full description

Saved in:
Bibliographic Details
Main Authors: Liu, Xiuxin (Author) , Titz, Stefan (Author) , Lewen, Andrea (Author) , Misgeld, Ulrich (Author)
Format: Article (Journal)
Language:English
Published: 1 October 2003
In: Journal of neurophysiology and neurological disorders
Year: 2003, Volume: 90, Issue: 4, Pages: 2785-2790
ISSN:2375-2491
DOI:10.1152/jn.00482.2003
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1152/jn.00482.2003
Verlag, lizenzpflichtig, Volltext: https://journals.physiology.org/doi/full/10.1152/jn.00482.2003
Get full text
Author Notes:Xiuxin Liu, Stefan Titz, Andrea Lewen, and Ulrich Misgeld
Description
Summary: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.
Item Description:Im Titel ist "4" tiefgestellt und "+" hochgestellt
Gesehen am 08.04.2021
Physical Description:Online Resource
ISSN:2375-2491
DOI:10.1152/jn.00482.2003