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

TitleBrain-derived neurotrophic factor rescues and prevents chronic intermittent hypoxia-induced impairment of hippocampal long-term synaptic plasticity
Authors
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
Citation
Neurobiology Of Disease, 2010, v. 40 n. 1, p. 155-162 How to Cite?
Abstract
Obstructive 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.
Persistent Identifierhttp://hdl.handle.net/10722/139664
ISSN
2013 Impact Factor: 5.202
ISI Accession Number ID
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).

References

 

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
DC FieldValueLanguage
dc.contributor.authorXie, Hen_HK
dc.contributor.authorLeung, KLen_HK
dc.contributor.authorChen, Len_HK
dc.contributor.authorChan, YSen_HK
dc.contributor.authorNg, PCen_HK
dc.contributor.authorFok, TFen_HK
dc.contributor.authorWing, YKen_HK
dc.contributor.authorKe, Yen_HK
dc.contributor.authorLi, AMen_HK
dc.contributor.authorYung, WHen_HK
dc.date.accessioned2011-09-23T05:53:11Z-
dc.date.available2011-09-23T05:53:11Z-
dc.date.issued2010en_HK
dc.identifier.citationNeurobiology Of Disease, 2010, v. 40 n. 1, p. 155-162en_HK
dc.identifier.issn0969-9961en_HK
dc.identifier.urihttp://hdl.handle.net/10722/139664-
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.en_HK
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ynbdien_HK
dc.relation.ispartofNeurobiology of Diseaseen_HK
dc.subjectBDNFen_HK
dc.subjectIntermittent hypoxiaen_HK
dc.subjectLTPen_HK
dc.subjectNeurotrophic factoren_HK
dc.subjectSleep apneaen_HK
dc.subjectSynaptic plasticityen_HK
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.titleBrain-derived neurotrophic factor rescues and prevents chronic intermittent hypoxia-induced impairment of hippocampal long-term synaptic plasticityen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0197-4580&volume=40&spage=155&epage=162&date=2010&atitle=Brain-derived+neurotrophic+factor+rescues+and+prevents+chronic+intermittent+hypoxia-induced+impairment+of+hippocampal+long-term+synaptic+plasticityen_US
dc.identifier.emailChan, YS: yschan@hkucc.hku.hken_HK
dc.identifier.authorityChan, YS=rp00318en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.nbd.2010.05.020en_HK
dc.identifier.pmid20553872en_HK
dc.identifier.scopuseid_2-s2.0-77955846318en_HK
dc.identifier.hkuros195166en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77955846318&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume40en_HK
dc.identifier.issue1en_HK
dc.identifier.spage155en_HK
dc.identifier.epage162en_HK
dc.identifier.isiWOS:000281473400019-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXie, H=36471439300en_HK
dc.identifier.scopusauthoridLeung, KL=37561685700en_HK
dc.identifier.scopusauthoridChen, L=15758988300en_HK
dc.identifier.scopusauthoridChan, YS=7403676627en_HK
dc.identifier.scopusauthoridNg, PC=7201376998en_HK
dc.identifier.scopusauthoridFok, TF=7006455238en_HK
dc.identifier.scopusauthoridWing, YK=7004821189en_HK
dc.identifier.scopusauthoridKe, Y=7102816469en_HK
dc.identifier.scopusauthoridLi, AM=7403291810en_HK
dc.identifier.scopusauthoridYung, WH=7103137893en_HK
dc.identifier.citeulike7271123-

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