Acidosis and blockade of orthodromic responses caused by anoxia in rat hippocampal slices at different temperatures.
1. Interstitial pH (pHo) and field responses (to stratum radiatum stimulation) were recorded simultaneously with double-barrelled microelectrodes in the CA1 region of hippocampal slices from Sprague-Dawley rats. 2. Both the relative acidity and amplitude of field responses increased with depth, reaching a maximum near the centre of the slice. When the temperature was raised from 22 to 37 degrees C, this pHo gradient was greater than 2 times steeper, but the field responses were much diminished. 3. Standard anoxic tests (substituting 95% N2 + 5% CO2 for 95% O2 + 5% CO2, for 2 min) tended to reduce pHo and population spikes, but these effects were highly temperature sensitive: at approximately 22 degrees C the blocking rate was only 12.3 +/- 4.6% and delta pHo -0.018 +/- 0.0157 units, both per minute; corresponding changes at 34-35 degrees C were 67.6 +/- 11.9% and -0.065 +/- 0.0046 units per minute. Highly significant linear correlations between rates of block and delta pHo gave a mean slope of 90.4 +/- 17.6% per 0.1 unit of acid change. 4. Anoxia caused similar temperature-dependent increases in acidity in stratum pyramidale and radiatum, but in the latter field responses (EPSPs) were much less depressed after 2 min of anoxia. 5. When slices were superfused with acid medium (low [HCO3-]), much greater reductions in pHo were needed to depress responses, giving a mean slope of 17.7% per 0.1 pH unit. 6. In glucose-free medium, there was a slow alkaline shift in pHo (0.13 +/- 0.036 units); population spikes and the acid transients evoked by anoxia disappeared. 7. It was concluded that acidosis cannot be the immediate cause of the similar depressions of postsynaptic excitability seen during anoxia and hypoglycaemia. 8. In further tests, DL-p-hydroxyphenyl-lactic acid, a blocker of lactate transport, failed to diminish acid transients evoked by anoxia, indicating that these are not mediated principally by lactate transport.
Krnjević
K
K
Anaesthesia Research Department, McGill University, Montréal, Québec, Canada.
Walz
W
W
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001639:Bicarbonates / Q000494:pharmacology; D005947:Glucose / Q000494:pharmacology; D006624:Hippocampus / Q000502:physiology*; D006358:Hot Temperature; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D009474:Neurons / Q000502:physiology*; D010100:Oxygen / Q000502:physiology*; D010666:Phenylpropionates / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains
D001639:Bicarbonates; D010666:Phenylpropionates; C001418:4-hydroxyphenyllactic acid; D005947:Glucose; D010100:Oxygen