1. Glutamate‐induced increases in intracellular free Ca2+ concentration ([Ca2+]i) were recorded from cultured rat hippocampal neurons with single cell microfluorometry. The [Ca2+]i increase did not correlate with glutamate‐induced cell death, consistent with the idea that Ca2+ accumulates in an intracellular store, and that loading this store might be toxic. 2. Glutamate‐induced Ca2+ loads were buffered by a low‐affinity, high‐capacity process that was inhibited by the mitochondrial uncoupling agent FCCP and modulated by intracellular Na+. 3. Glutamate‐induced Ca2+ loads also produced an intracellular acidification. The acidification was prevented by the metabolic inhibitor 2‐deoxyglucose, mimicked by Ba2+, and inhibited by microinjection of ruthenium red. 4. These data are consistent with the hypothesis that mitochondria sequester glutamate‐induced Ca2+ loads producing a metabolic acidosis; metabolic stress may contribute to glutamate‐induced neuronal death.
|Original language||English (US)|
|Number of pages||2|
|Journal||Clinical and Experimental Pharmacology and Physiology|
|State||Published - Apr 1995|
- intracellular calcium
- intracellular pH