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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.

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