About: A HIF1a-Dependent Pro-Oxidant State Disrupts Synaptic Plasticity and Impairs Spatial Memory in Response to Intermittent Hypoxia

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About: A HIF1a-Dependent Pro-Oxidant State Disrupts Synaptic Plasticity and Impairs Spatial Memory in Response to Intermittent Hypoxia Goto Sponge NotDistinct Permalink

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	A HIF1a-Dependent Pro-Oxidant State Disrupts Synaptic Plasticity and Impairs Spatial Memory in Response to Intermittent Hypoxia
Creator	Arias-Cavieres, Alejandra Barnard, Jasmine Dalgin, Gokhan Khuu, Maggie Nwakudu, Chinwendu Iii, Alfredo
Source	PMC
abstract	Sleep apnea causes cognitive deficits and is associated with several neurologic diseases. Intermittent hypoxia (IH) is recognized as a principal mediator of pathophysiology associated with sleep apnea, yet the basis by which IH contributes to impaired cognition remains poorly defined. Using a mouse model exposed to IH, this study examines how the transcription factor, hypoxia inducible factor 1a (HIF1a), contributes to disrupted synaptic physiology and spatial memory. In wild-type mice, impaired performance in the Barnes maze caused by IH coincided with a loss of NMDA receptor (NMDAr)-dependent long-term potentiation (LTP) in area CA1 and increased nuclear HIF1a within the hippocampus. IH-dependent HIF1a signaling caused a two-fold increase in expression of the reactive oxygen species (ROS) generating enzyme NADPH oxidase 4 (NOX4). These changes promoted a pro-oxidant state and the downregulation of GluN1 within the hippocampus. The IH-dependent effects were not present in either mice heterozygous for Hif1a (HIF1a(+/−)) or wild-type mice treated with the antioxidant manganese (III) tetrakis(1-methyl-4-pyridyl) porphyrin (MnTMPyP). Our findings indicate that HIF1a-dependent changes in redox state are central to the mechanism by which IH disrupts hippocampal synaptic plasticity and impairs spatial memory. This mechanism may enhance the vulnerability for cognitive deficit and lower the threshold for neurologic diseases associated untreated sleep apnea.
has issue date	2020-06-19(xsd:dateTime)
bibo:doi	10.1523/eneuro.0024-20.2020
bibo:pmid	32493757
has license	cc-by
sha1sum (hex)	135691c0ddec236a84513b0b16fd4987b43df17c
schema:url	https://doi.org/10.1523/eneuro.0024-20.2020
resource representing a document's title	A HIF1a-Dependent Pro-Oxidant State Disrupts Synaptic Plasticity and Impairs Spatial Memory in Response to Intermittent Hypoxia
has PubMed Central identifier	PMC7363479
has PubMed identifier	32493757
schema:publication	eNeuro
resource representing a document's body	covid:135691c0ddec236a84513b0b16fd4987b43df17c#body_text
is schema:about of	named entity 'neurologic diseases' named entity 'mice' named entity 'hippocampus' named entity 'sleep apnea' named entity 'redox' named entity 'Plasticity' named entity 'heterozygous' named entity 'NMDAr' named entity 'hippocampus' named entity 'The' named entity 'porphyrin' named entity 'hypoxia inducible factor' named entity 'hypoxia inducible factor 1a' named entity 'antioxidant' named entity 'NOX4' named entity 'neurologic diseases' named entity 'reactive oxygen species' named entity 'mice' named entity 'long-term potentiation' named entity 'HIF1a' named entity 'manganese' named entity 'HIF1a' named entity 'wild-type' named entity 'mice' named entity 'spatial memory' named entity 'heterozygous' named entity 'HIF1a' named entity 'NMDA' named entity 'cognitive deficit' named entity 'wild-type' named entity 'Synaptic Plasticity' named entity 'synaptic physiology' named entity 'enzyme' named entity 'downregulation' named entity 'Spatial Memory' named entity 'tetrakis' named entity 'pro-oxidant' named entity 'HIF1a' named entity 'Our' named entity 'synaptic plasticity' named entity 'Hypoxia' named entity 'OUR' named entity 'EXPRESSION' named entity 'HOW' named entity 'DEPENDENT' named entity 'COGNITIVE DEFICITS' named entity 'ENZYME' named entity 'IMPAIRED COGNITION' named entity 'DOWNREGULATION' named entity 'THRESHOLD' named entity 'THESE' named entity 'impaired cognition' named entity 'cognitive deficits' named entity 'LTP' named entity 'sleep apnea' named entity 'GluN1' named entity 'ROS' named entity 'redox' named entity 'NADPH oxidase 4' named entity 'hippocampal' named entity 'receptor' named entity 'hypoxia' named entity 'Hif1a' named entity 'Sleep apnea' named entity 'mouse model' named entity 'hippocampus' named entity 'transcription factor' named entity 'pro-oxidant' named entity 'Pro-Oxidant' named entity 'GLUN1' named entity '4-PYRIDYL' named entity 'ASSOCIATED' named entity 'LONG-TERM POTENTIATION' named entity 'HIPPOCAMPAL' named entity 'FOLD INCREASE' named entity 'NOT PRESENT'

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