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Temperature is regulated in hibernating Syrian hamsters at temperatures that selectively suppress hippocampal neural mechanisms underlying memory formation
Author(s) -
Gill Phoebe D,
Horowitz John M,
Hamilton Jock S,
Horwitz Barbara A
Publication year - 2007
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.21.6.a1312-d
Subject(s) - hippocampal formation , long term potentiation , neuroscience , brainstem , hibernation (computing) , population , chemistry , population spike , hamster , biology , endocrinology , medicine , dentate gyrus , biochemistry , state (computer science) , algorithm , computer science , receptor , environmental health
Previous studies demonstrate that hibernators continue to regulate core temperature in hibernation, even at very low body temperature. We hypothesized that although hippocampal signals activating cellular mechanisms (long term potentiation, LTP) for the formation of memories are inhibited when the hamster hibernates, hippocampal signaling persists to suppress brainstem arousal systems, which in turn, could influence the duration of a hibernation bout. To test this hypothesis, we measured tetanus‐induced LTP and the dispersion of a packet of action potentials through a network of CA1 pyramidal cells. Below a temperature threshold of 18°C, LTP following tetanus could not be established (n = 4), while above 18°C it was readily generated (n =10). In contrast, population spikes (PS) could be evoked at 15°C. In slices from 10 euthermic hamsters, the latency from stimulus to PS peak was 14.6 + 1.0 msec (mean + SEM, p<.001); and PS half‐max duration was 4.3 + 0.4 msec. In 7 slices from hibernating hamsters, similar changes were observed (latency to PS of 16.0 + 0.8, and PS half‐max duration of 5.6 + 0.6). These findings are consistent with our hypothesis that at temperatures at and below 18°C, hibernators selectively switch off neural network properties supporting memory formation while preserving signal transmission over hippocampal circuits to modulate brainstem networks that can control the duration of the hibernation bouts.