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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
2013 Impact Factor: 5.202
 
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 FieldValue
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
2013 Impact Factor: 5.202
 
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
 
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<contributor.author>Chen, L</contributor.author>
<contributor.author>Chan, YS</contributor.author>
<contributor.author>Ng, PC</contributor.author>
<contributor.author>Fok, TF</contributor.author>
<contributor.author>Wing, YK</contributor.author>
<contributor.author>Ke, Y</contributor.author>
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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