Abstract

Previous studies showed that CA1 pyramidal cells in the hippocampus of nonhibernating and hibernating Syrian hamsters (Mesocricetus auratus) exhibit greater neuroprotection at 30°C than do those of rats. However, the temperature dependence of the hamster neurons to an anoxic insult has not been studied. We tested the hypothesis that the effect of anoxic exposure on population spike amplitude (PSA) following Shaffer‐collateral/commissural stimulation is attenuated with decreasing temperature. In slices from euthermic hamsters, CA1 pyramidal cell PSA was measured every minute throughout the experiment. Following a 15 minute control period in oxygenated (95%O2/5%CO2) buffer, oxygen was replaced with nitrogen (95%N2/5%CO2) for 15 minutes (the anoxic insult). Oxygenated buffer was then returned to the slices for a 30 minute recovery period. Three minutes after nitrogen exposure at 35°C, PSA had a 75.1 ± 14.9% (mean ± SE) drop from control, compared to a smaller drop (20.3 ± 5.3%) at 30°C. Three minutes after return to oxygenated buffer at 35°C, PSA had recovered by only 5.7 ± 2.9% compared with a 62.4 ± 6.8% recovery at 30°C. Differences are significant (P<0.05), consistent with our hypothesis, and consistent with the proposal that neuroprotection in CA1 pyramidal cells increased as temperature decreased.

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