Premium
Lowered set‐point for hypothalamic temperature regulation alters hippocampal activity and may enhance neuroprotection in hibernating hamsters
Author(s) -
Goo Marisa S,
Nguyen Yen H,
Becker Jeffrey J,
Hamilton Jock S,
Horowitz John M
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.956.16
Subject(s) - hippocampal formation , long term potentiation , neuroprotection , hibernation (computing) , torpor , nmda receptor , endocrinology , medicine , population spike , neuroscience , glutamate receptor , chemistry , population , stimulation , biology , thermoregulation , dentate gyrus , receptor , state (computer science) , environmental health , algorithm , computer science
The hypothalamus regulates temperature in hibernators at all stages of the hibernation cycle. Thus, in addition to direct neural signaling, it may modify neural activity in other CNS regions via its regulation of low brain temperatures. We hypothesized that as temperature falls and hamsters enter hibernation, hippocampal NMDAR channels are arrested, minimizing potential excitotoxic cell damage. To test this hypothesis, we measured in hippocampal slices the generation of long‐term potentiation (LTP), which requires Ca 2+ influx through NMDAR channels to activate the process; and dispersion and amplitude of population spikes (PS), because synchronized activity is required to gate NMDARs. Although LTP following tetanus was readily generated (n=10) above 18°C, it could not be established below 18°C (n = 4). In slices from 10 euthermic hamsters, PS amplitude decreased from 1.6 ± 0.1 at 25°C to 0.9 ± 0.1 mV at 15°C; and PS half‐max duration increased from 1.7 ± 0.1 to 4.3 ± 0.4 msec (mean ± SEM, p<.001). In 7 slices from hibernating hamsters, similar changes were seen (PS amplitude fell from 2.1 ± 0.2 to 0.8 ± 0.2 at 15°C, and PS half‐max duration rose from 1.8 ± 0.1 to 5.6 ± 0.6, p<.001). These data are consistent with our hypothesis that cellular pathways activated by Ca 2+ influx through NMDARs are silenced in hibernating hamsters and may contribute to neuroprotection during hibernation. (Supported in part by a PUF grant to M.G.)