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Disrupted spatial learning and memory is unaffected by training prior to intermittent hypoxia exposure
Author(s) -
Nwakudu Chinwendu U.,
AriasCavieres Alejandra,
Khuu Maggie A.,
Garcia Alfredo J.
Publication year - 2019
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.2019.33.1_supplement.551.22
Subject(s) - hippocampal formation , intermittent hypoxia , latency (audio) , psychology , spatial learning , memory formation , analysis of variance , cognitive training , water maze , neuroscience , long term potentiation , barnes maze , spatial memory , audiology , cognition , medicine , anesthesia , working memory , obstructive sleep apnea , computer science , telecommunications , receptor
Intermittent hypoxia (IH) is a common event occurring with untreated sleep apnea, a clinical condition commonly associated with cognitive deficits in learning and memory. Rodents exposed to IH, as a model for sleep apnea, exhibit impairments in spatial learning and memory. However, performance on spatial learning and memory tasks show individual variance. The objective of this ongoing study is to determine whether training prior to IH exposure influences performance on spatial learning tasks following IH. We hypothesize that while IH impairs spatial learning and memory through an oxidative stress mediated mechanism, training prior to exposure will improve performance on spatial memory tasks following IH. To test this, we developed a Barnes maze protocol to assess spatial learning and memory in mice preceding and after exposure to 10 days of IH (IH10). Before IH10, variance among individual mice was evident during the probe trial in the latency to initial entry into the exit zone. However, during the second maze session (10 days after the first probe trial), the latency in initial entry into the exit zone was increased in IH10 treated mice (n=4). Conversely, mice naive to IH10 exhibited decreased latency in initial entry into the exit zone during the second maze session (n=4). LTP measured in area CA1 was suppressed in hippocampal brain slices from mice exposed to IH (control 162%±12% (n=7) vs. IH 122±7% (n=11)). This suppression of LTP was only partially mitigated by antioxidant treatment during IH10. These results indicate that IH disrupts learning and memory independent of prior training and impaired spatial learning and memory corresponds with suppressed LTP following IH. Support or Funding Information This work was supported by NIH R01 NS10742101 (AJG) This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .