Bicarbonate efflux via GABA(A) receptors depolarizes membrane potential and inhibits two-pore domain potassium channels of astrocytes in rat hippocampal slices.

ABSTRACT: Increasing evidence indicates the functional expression of ionotropic γ-aminobutyric acid receptor (GABA(A) -R) in astrocytes. However, it remains controversial in regard to the intracellular Cl(-) concentration ([Cl(-) ](i) ) and the functional role of anion-selective GABA(A) -R in astrocytes. In gramicidin perforated-patch recordings from rat hippocampal CA1 astrocytes, GABA and GABA(A) -R-specific agonist THIP depolarized astrocyte membrane potential (V(m) ), and the THIP-induced currents reversed at the voltages between -75.3 and -78.3 mV, corresponding to a [Cl(-) ](i) of 3.1-3.9 mM that favored a passive distribution of Cl(-) anions across astrocyte membrane. Further analysis showed that GABA(A) -R-induced V(m) depolarization was ascribed to HCO(3) (-) efflux, while a passively distr

SUBMITTER: Ma BF 

PROVIDER: S-EPMC3901573 | biostudies-literature | 2012 Nov

REPOSITORIES: biostudies-literature