Abstract
The role of extracellular endogenous gamma-aminobutyric acid (GABA) in rescuing retinal cells in culture from the decrease in viability induced by Glu under metabolic inhibition is analyzed. Glutamate (10 microM-10 mM) dose-dependently decreased the intracellular GABA content, but increased the extracellular accumulation of GABA. In the absence of glucose, Glu (10-100 microM) decreased the intracellular GABA (2-fold), whereas the extracellular accumulation of GABA was increased by about 4-fold. Glu-mediated decrement in cell survival was not affected by inhibiting the GABA(A) receptors with bicuculline (1 or 10 microM) or by blocking the Na+ -dependent release of GABA with 1-(4,4-diphenyl-3-butenyl)-3-piperidinecarboxylic acid (SKF89976-A). Data suggest a non-protective role of endogenous GABA release after metabolic deprivation of retinal cells submitted to Glu.
Published Version
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