Article: Brain-derived neurotrophic factor rescues and prevents chronic intermittent hypoxia-induced impairment of hippocampal long-term synaptic plasticity

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TitleBrain-derived neurotrophic factor rescues and prevents chronic intermittent hypoxia-induced impairment of hippocampal long-term synaptic plasticity
AuthorsXie, H3
Leung, KL3
Chen, L2 3
Chan, YS1
Ng, PC3
Fok, TF3
Wing, YK3
Ke, Y3
Li, AM3
Yung, WH3
KeywordsBDNF
Intermittent hypoxia
LTP
Neurotrophic factor
Sleep apnea
Synaptic plasticity
Issue Date2010
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ynbdi
CitationNeurobiology Of Disease, 2010, v. 40 n. 1, p. 155-162 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.nbd.2010.05.020
AbstractObstructive sleep apnea (OSA) is a common sleep and breathing disorder characterized by repeated episodes of hypoxemia. OSA causes neurocognitive deficits including perception and memory impairment but the underlying mechanisms are unknown. Here we show that in a mouse model of OSA, chronic intermittent hypoxia treatment impairs both early- and late-phase long-term potentiation (LTP) in the hippocampus. In intermittent hypoxia-treated mice the excitability of CA1 neurons was reduced and hippocampal brain-derived neurotrophic factor (BDNF) was down-regulated. We further showed that exogenous application of BDNF restored the magnitude of LTP in hippocampal slices from hypoxia-treated mice. In addition, microinjection of BDNF into the brain of the hypoxic mice prevented the impairment in LTP. These data suggest that intermittent hypoxia impairs hippocampal neuronal excitability and reduces the expression of BDNF leading to deficits in LTP and memory formation. Thus, BDNF level may be a novel therapeutic target for alleviating OSA-induced neurocognitive deficits. © 2010 Elsevier Inc.
ISSN0969-9961
2011 Impact Factor: 5.403
2011 SCImago Journal Rankings: 0.506
DOIhttp://dx.doi.org/10.1016/j.nbd.2010.05.020
ISI Accession Number IDWOS:000281473400019
Funding AgencyGrant Number
Research Grants Council of Hong Kong478308
CUHK4527/06M
Funding Information:

This study was supported by grants from the Research Grants Council of Hong Kong (Project No. 478308 and CUHK4527/06M).

ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorXie, H
dc.contributor.authorLeung, KL
dc.contributor.authorChen, L
dc.contributor.authorChan, YS
dc.contributor.authorNg, PC
dc.contributor.authorFok, TF
dc.contributor.authorWing, YK
dc.contributor.authorKe, Y
dc.contributor.authorLi, AM
dc.contributor.authorYung, WH
dc.date.accessioned2011-09-23T05:53:11Z
dc.date.available2011-09-23T05:53:11Z
dc.date.issued2010
dc.description.abstractObstructive sleep apnea (OSA) is a common sleep and breathing disorder characterized by repeated episodes of hypoxemia. OSA causes neurocognitive deficits including perception and memory impairment but the underlying mechanisms are unknown. Here we show that in a mouse model of OSA, chronic intermittent hypoxia treatment impairs both early- and late-phase long-term potentiation (LTP) in the hippocampus. In intermittent hypoxia-treated mice the excitability of CA1 neurons was reduced and hippocampal brain-derived neurotrophic factor (BDNF) was down-regulated. We further showed that exogenous application of BDNF restored the magnitude of LTP in hippocampal slices from hypoxia-treated mice. In addition, microinjection of BDNF into the brain of the hypoxic mice prevented the impairment in LTP. These data suggest that intermittent hypoxia impairs hippocampal neuronal excitability and reduces the expression of BDNF leading to deficits in LTP and memory formation. Thus, BDNF level may be a novel therapeutic target for alleviating OSA-induced neurocognitive deficits. © 2010 Elsevier Inc.
dc.description.natureLink_to_subscribed_fulltext
dc.identifier.citationNeurobiology Of Disease, 2010, v. 40 n. 1, p. 155-162 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.nbd.2010.05.020
dc.identifier.citeulike7271123
dc.identifier.doihttp://dx.doi.org/10.1016/j.nbd.2010.05.020
dc.identifier.epage162
dc.identifier.hkuros195166
dc.identifier.isiWOS:000281473400019
Funding AgencyGrant Number
Research Grants Council of Hong Kong478308
CUHK4527/06M
Funding Information:

This study was supported by grants from the Research Grants Council of Hong Kong (Project No. 478308 and CUHK4527/06M).

dc.identifier.issn0969-9961
2011 Impact Factor: 5.403
2011 SCImago Journal Rankings: 0.506
dc.identifier.issue1
dc.identifier.openurl
dc.identifier.pmid20553872
dc.identifier.scopuseid_2-s2.0-77955846318
dc.identifier.spage155
dc.identifier.urihttp://hdl.handle.net/10722/139664
dc.identifier.volume40
dc.languageeng
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ynbdi
dc.publisher.placeUnited States
dc.relation.ispartofNeurobiology of Disease
dc.relation.referencesReferences in Scopus
dc.subject.meshBrain-Derived Neurotrophic Factor - administration and dosage - therapeutic use
dc.subject.meshHippocampus - drug effects - metabolism - physiopathology
dc.subject.meshHypoxia, Brain - metabolism - physiopathology - prevention and control
dc.subject.meshNeuronal Plasticity - physiology
dc.subject.meshSynapses - physiology
dc.subjectBDNF
dc.subjectIntermittent hypoxia
dc.subjectLTP
dc.subjectNeurotrophic factor
dc.subjectSleep apnea
dc.subjectSynaptic plasticity
dc.titleBrain-derived neurotrophic factor rescues and prevents chronic intermittent hypoxia-induced impairment of hippocampal long-term synaptic plasticity
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. Qingdao University, School of Medicine
  3. Chinese University of Hong Kong