KCC2 mediates NH4+ uptake in cultured rat brain neurons

• Verfasst von: Liu, Xiuxin [VerfasserIn]
• Verfasst von: Titz, Stefan [VerfasserIn]
• Verfasst von: Lewen, Andrea [VerfasserIn]
• Verfasst von: Misgeld, Ulrich [VerfasserIn]
• Titel: KCC2 mediates NH4+ uptake in cultured rat brain neurons
• Verf.angabe: Xiuxin Liu, Stefan Titz, Andrea Lewen, and Ulrich Misgeld
• E-Jahr: 2003
• Jahr: 1 October 2003
• Umfang: 6 S.
• Teil: volume:90
• Teil: year:2003
• Teil: number:4
• Teil: pages:2785-2790
• Teil: extent:6
• Fussnoten: Im Titel ist "4" tiefgestellt und "+" hochgestellt ; Gesehen am 08.04.2021
• Titel Quelle: Enthalten in: Journal of neurophysiology and neurological disorders
• Ort Quelle: Sunnyvale : JScholar Online Publishers, 2013
• Jahr Quelle: 2003
• Band/Heft Quelle: 90(2003), 4, Seite 2785-2790
• ISSN Quelle: 2375-2491
• DOI: doi:10.1152/jn.00482.2003
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1753322464

Abstract

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.