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Long‐Term Potentiation (LTP) in Syrian Hamster Hippocampal Slices Can Be Generated at Warm (35[deg]C[endash]20[deg]C) but Not Cool (15[deg]C) Slice Temperatures over a Hibernation Cycle
Author(s) -
Horowitz John M,
Hamilton Jock S,
Chau Sat M,
Horwitz Barbara A
Publication year - 2017
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.31.1_supplement.861.8
Subject(s) - long term potentiation , hamster , population spike , hippocampal formation , torpor , hibernation (computing) , population , stimulation , chemistry , biology , neuroscience , endocrinology , medicine , thermoregulation , biochemistry , state (computer science) , receptor , environmental health , algorithm , computer science
Previous studies have shown that LTP, a form of synaptic plasticity supporting the formation of memories, can be generated in the Syrian hamster, a facultative hibernator. However, the full range of brain temperatures at which LTP can be generated at various times of the hibernation cycle has yet to be fully delineated. We hypothesized that LTP in hamsters prepared to enter hibernation could be generated at lower temperatures than in hamsters not prepared to hibernate. To test this hypothesis, we compared responses of slices from non‐hibernating hamsters housed in a summer‐like environment (SH slices), to responses of slices from hamsters housed in a winter‐like environment but had not yet entered torpor (WH slices), and to slices from hamsters housed in a winter‐like environment that had entered torpor (HH slices). For this, we measured tetanus‐induced LTP [a sustained enhancement of population spike (PS) amplitude] and the dispersion of a packet of action potentials over a network of CA1 pyramidal cells [the width of a PS]. In all three groups, we observed sustained enhancement of PS amplitude lasting at least 1 hour, the hallmark of LTP generation, at temperatures above 20°C. However, no enhancement was seen at or below 15°C in any group. Moreover, at 15°C, synchronization of pyramidal cell firing following single‐shock stimulation, necessary for LTP generation, was degraded – i.e., PS width at 15°C was 5 times that observed at 35°C. Overall, our data negate our hypothesis and suggest that new memories cannot be formed via LTP synaptic enhancement during the late stages of entry into hibernation, during hibernation itself, or during the early stages of arousal from hibernation. Additionally, our results from the SH and WH slices imply that LTP may be a major cellular plasticity mechanism underlying the finding that hamsters that master a hippocampal behavioral task prior to hibernation can execute the task after hibernation. That is, LTP changes occurring at postsynaptic sites before hibernation persist through a series of hibernation bouts (and changes in dendritic spine structure) to a degree sufficient to allow hamsters to perform the task upon arousal.