Abstract

Previous studies showed that the neuromodulator histamine (HA) increases hibernation bout duration and, in non‐hibernating species, attenuates ischemic neuronal damage. We tested the hypotheses that: (1) HA directly enhances CA1 and CA3 Syrian hamster (Mesocricetus auratus) pyramidal cell excitability and (2) HA promotes recovery from an anoxic insult. HA (10μM) was applied directly to hippocampal slices and evoked responses (ERs) were recorded before, during, and after HA perfusion at 30ºC. ERs were also recorded before, during, and after a 15 min anoxic insult (95%N2/5%CO2). We found that HA increased ERs recorded from the CA1 region (23% increase, P< 0.05) and shortened the latency to the ER peaks (16–26% decrease, P<0.01) in 7 slices from 5 hamsters. In the CA3 region, HA had similar, though smaller, effects on latency and amplitude. Following anoxia, in the presence of HA, 5 slices recovered faster, 2 slower, and 1 was unaffected vs. slices without HA. Data are consistent with both hypotheses and suggest that HA has multiple, synergistic effects on pyramidal cells. Moreover, the observed HA‐induced enhanced excitability of pyramidal cells supports the view that these cells play a key role in the neural pathway regulating hibernation bout duration. The increased rate of recovery suggests that HA also has a neuroprotective role, ensuring reliable signal processing in a hibernating hamster.

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