In this study we investigated in rat hippocampal slices (1) how
glucose availability affected tissue
acidosis during and after
anoxia, (2) whether the onset of anoxic depolarization was associated with a specific
pH, (3) whether glycolysis was the major source of acidification before and during anoxic depolarization, and (4) whether improved recovery of synaptic function with elevated
glucose levels was related to changes in tissue
acidosis. Intracellular pH (pHi) and extracellular pH (pHo) were measured simultaneously before, during, and after
anoxia in hippocampal slices bathed in 0, 5, 10, and 15 mM
glucose. Slices exposed to 0 mM
glucose were given 20 mM
sodium lactate as a metabolic substrate. We found that the pHi and pHo at which anoxic depolarization occurred depended upon
glucose concentration. We also found that elevated
glucose availability increased acidification in both the intracellular and extracellular compartments during
anoxia and delayed recovery of pH homeostasis after
anoxia. Our results suggest that glycolysis is the primary source of
acidosis before the onset of anoxic depolarization, but not during anoxic depolarization. Our results also suggest that moderate increases in
acidosis resulting from increased glycolysis are potentially beneficial for anoxic survival.