Recovery of Syrian hamster hippocampal signaling following its depression during oxygen-glucose deprivation is enhanced by cold temperatures and by hibernation

• Published in: Neuroscience letters 2016-05, Vol.621, p.98-103
• Main Authors: Mikhailova, Alexandra, Mack, Jacob, Vitagliano, Nicholas, Hamilton, Jock S., Horowitz, John M., Horwitz, Barbara A.
• Format: Article
• Language: English
• Subjects: Animals; CA1 pyramidal cells; CA1 Region, Hippocampal - metabolism; CA1-CA3 synapse; CA3 Region, Hippocampal - metabolism; Cold Temperature; Cricetinae; Depression - physiopathology; fEPSP; Glucose - deficiency; Hibernati; Hibernation; Hippocampus - physiopathology; Mesocricetus; Mesocricetus auratus; Oxygen - metabolism; Oxygen deprivation; Population spike; Signal Transduction; Synapses - metabolism
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2016.04.011

[Display omitted] •During OGD signaling is attenuated within minutes by CA3-CA1 synaptic mechanisms.•After OGD, signaling recovers more quickly and fully in hamsters than in rats.•Recovery in signaling is more robust in hibernating than nonhibernating hamsters.•Signaling in hamster neurons has protective mechanisms providing tolerance to OGD. Signal transmission over a hippocampal network of CA3 and CA1 neurons in Syrian hamsters (Mesocricetus auratus), facultative hibernators, has not been fully characterized in response to oxygen-glucose deprivation (OGD). We hypothesized that during OGD, hippocampal signal transmission fails first at the synapse between CA3 and CA1 pyramidal neurons and that recovery of signal processing following OGD is more robust in hippocampal slices at cold temperature, from hamsters vs. rats, and from hibernating vs. non-hibernating hamsters. To test these hypotheses, we recorded fEPSPs and population spikes of CA1 neurons at 25°C, 30°C, and 35°C in 400μm slices over a 15min control period with the slice in oxygenated aCSF containing glucose (control solution), a 10min treatment period (OGD insult) where oxygen was replaced by nitrogen in aCSF lacking glucose, and a 30min recovery period with the slice in the control solution. The initial site of transmission failure during OGD occurred at the CA3-CA1 synapse, and recovery of signal transmission was at least, if not more (depending on temperature), complete in slices from hibernating vs. non-hibernating hamsters, and from non-hibernating hamsters vs. rats. Thus, hamster neuroprotective mechanisms supporting functional recovery were enhanced by cold temperatures and by hibernation.