Effect of lactic and CO2 acidosis on neuronal function following glucose-oxygen deprivation in rat hippocampal slices.

The present study was designed to determine whether lactate changes the critical pH point at which the recovery of rat population spike is inhibited following glucose-oxygen deprivation and second, which degree of lactic acidosis is similar to the effect of CO2 acidosis. The population spike was recorded from the hippocampal CA1 region after stimulation of the Schaffer collaterals. Slices were randomly perfused with various acidotic solutions for 30 min. During the last 15 min, glucose-oxygen deprivation was combined with the acidotic perfusion. Then the hippocampal slices were perfused with a standard solution of pH 7.4 for 60 min and recovery was compared to the control population spike and expressed as a percentage of the control value. In the control acidotic solution, the critical pH point was 5.0. When 15 mM or 30 mM lactate were added to the control solution, the critical pH point changed to 5.5 or 6.0, suggesting that the inhibition of the population spike was enhanced by lactate in a dose-dependent fashion. The recovery of the population spike was inhibited by exposing the slices to CO2 of 25% or above (pH was 5.76 or below) and this inhibition of recovery associated with CO2 acidosis was the same degree as occurred with 30 mM, namely severe lactic acidosis.