Recovery of synaptic transmission following oxygen glucose deprivation (OGD) in the Syrian hamster hippocampus is enhanced at lower temperatures

Abstract

We previously found neural networks in Syrian hamsters, a hibernating species, to be more tolerant to oxygen deprivation (OD) than rats. Here we describe effects of OGD on hamster neural activity under conditions more closely approximating stroke. We hypothesized that exposure of hamster hippocampal slices to OGD impairs neural activity (slows recovery) more than does OD, and that decreased temperature speeds recovery. Evoked response amplitudes (ERAs) of CA1 neurons to afferent stimulation were measured each minute of a 15 min control period [slices perfused with oxygenated artificial cerebrospinal fluid (O2 aCSF, 10 mM glucose)]; during treatment (perfusate switched to aCSF gassed with nitrogen and no glucose) for either 10 or 15 min; and during recovery (slices returned to O2 aCSF, 10 mM glucose for 30 min). At 25°C, 5 min after 15 min of OD, ERAs recovered to 84.4 ± 9.2% of control while OGD‐treated slices recovered to 61.0 ± 14.0% (P<0.05). Thus, at 25°C, recovery from OGD was more impaired than that from OD. Lower slice temperatures significantly shortened recovery time (P<0.05), such that at 5 min recovery after a 10 min ODG exposure, ERAs returned to 36% of control at 35°C, 77% of control at 30°C, and 96% of control at 25°C. In summary, these data support our hypothesis that OGD exposure is more damaging than OD, and that lowering temperature enhances recovery. (Supported by a President's Undergraduate Fellowship to AM)