Beschreibung:
<jats:p>Previous studies showed that neurons in mammalian obligatory hibernators are less damaged by oxygen glucose deprivation (OGD) than those of non‐hibernating species. But it is unknown if recovery of hippocampal signal processing after transient OGD is greater in facultative hibernators (e.g., Syrian hamsters) than in rats (non‐hibernators). We tested the hypotheses that 30 min after OGD exposure, recovery would be greater: (1) at low vs. high temperatures in both species and (2) in hamsters vs. rats. Following Schaffer collateral stimulation, evoked responses from CA1 neurons were measured at 25<jats:sup>o</jats:sup>C, 30<jats:sup>o</jats:sup>C, and 35<jats:sup>o</jats:sup>C. A 15 min baseline response was recorded for slices perfused in oxygenated artificial cerebrospinal fluid (O<jats:sub>2</jats:sub>aCSF). Perfusate was then switched to aCSF minus glucose and gassed with nitrogen (OGD) for 10 min, after which it was returned to O<jats:sub>2</jats:sub>aCSF for 30 min. Degree of recovery from OGD was significantly greater (P<0.05) at lower temperatures in hamster and rat slices, supporting hypothesis 1. Additionally, at 25<jats:sup>o</jats:sup>C, hamster slice recovery (108%; n=19 slices) was significantly greater (P<0.05) than that of rat slices (80%; n= 16). The same was true at 30<jats:sup>o</jats:sup>C (93% for 19 hamster slices vs. 49% for 18 rat slices), consistent with hypothesis 2. <jats:italic>No significant species differences were seen at 35<jats:sup>o</jats:sup>C.</jats:italic> Understanding naturally occurring tolerance to OGD in hibernators may lead to new strategies mitigating stroke damage.</jats:p><jats:p><jats:bold><jats:italic>Grant Funding Source</jats:italic></jats:bold><jats:italic>: JM was supported by an American Physiological Society UGSRF award.</jats:italic></jats:p>