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Article: Absence of MK801-induced inspiratory prolongation in chronically hypoxic rats

TitleAbsence of MK801-induced inspiratory prolongation in chronically hypoxic rats
Authors
Issue Date2001
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie
Citation
Life Sciences, 2001, v. 69 n. 19, p. 2319-2326 How to Cite?
AbstractN-methyl-D-aspartate (NMDA) receptors play important roles in the neural control of respiration. We hypothesized that the brainstem circuit for respiratory control is modulated in response to chronic hypoxia during postnatal maturation, and the modulation may involve changes in the neurotransmission mediated by the NMDA receptors for inspiratory termination. Electrophysiological studies were performed on anesthetized, vagotomized, paralyzed and ventilated rats. Phrenic nerve activity was recorded in normoxic control and chronically hypoxic (CH) rats maintained in normobaric hypoxia (10% O 2) for 4-5 weeks from birth. In normoxic rats, the NMDA receptor antagonist, dizocilpine (MK801, I.P.) irreversibly increased inspiratory time (Ti) by 53% and decreased expiratory time (Te) by 29%. However, MK801 did not change the Ti, Te, respiratory rate and peak phrenic nerve activity in CH rats. Results suggest that brainstem mechanisms underlying inspiratory termination mediated by NMDA receptors are modulated by early chronic hypoxia. © 2001 Elsevier Science Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/171702
ISSN
2015 Impact Factor: 2.685
2015 SCImago Journal Rankings: 1.056
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFung, MLen_US
dc.contributor.authorDong, Xen_US
dc.date.accessioned2012-10-30T06:16:29Z-
dc.date.available2012-10-30T06:16:29Z-
dc.date.issued2001en_US
dc.identifier.citationLife Sciences, 2001, v. 69 n. 19, p. 2319-2326en_US
dc.identifier.issn0024-3205en_US
dc.identifier.urihttp://hdl.handle.net/10722/171702-
dc.description.abstractN-methyl-D-aspartate (NMDA) receptors play important roles in the neural control of respiration. We hypothesized that the brainstem circuit for respiratory control is modulated in response to chronic hypoxia during postnatal maturation, and the modulation may involve changes in the neurotransmission mediated by the NMDA receptors for inspiratory termination. Electrophysiological studies were performed on anesthetized, vagotomized, paralyzed and ventilated rats. Phrenic nerve activity was recorded in normoxic control and chronically hypoxic (CH) rats maintained in normobaric hypoxia (10% O 2) for 4-5 weeks from birth. In normoxic rats, the NMDA receptor antagonist, dizocilpine (MK801, I.P.) irreversibly increased inspiratory time (Ti) by 53% and decreased expiratory time (Te) by 29%. However, MK801 did not change the Ti, Te, respiratory rate and peak phrenic nerve activity in CH rats. Results suggest that brainstem mechanisms underlying inspiratory termination mediated by NMDA receptors are modulated by early chronic hypoxia. © 2001 Elsevier Science Inc. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescieen_US
dc.relation.ispartofLife Sciencesen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnoxia - Physiopathologyen_US
dc.subject.meshDizocilpine Maleate - Pharmacologyen_US
dc.subject.meshExcitatory Amino Acid Antagonists - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshReceptors, N-Methyl-D-Aspartate - Physiologyen_US
dc.subject.meshRespiration - Drug Effectsen_US
dc.titleAbsence of MK801-induced inspiratory prolongation in chronically hypoxic ratsen_US
dc.typeArticleen_US
dc.identifier.emailFung, ML:fungml@hkucc.hku.hken_US
dc.identifier.authorityFung, ML=rp00433en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0024-3205(01)01319-4en_US
dc.identifier.pmid11669474-
dc.identifier.scopuseid_2-s2.0-0035964908en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035964908&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume69en_US
dc.identifier.issue19en_US
dc.identifier.spage2319en_US
dc.identifier.epage2326en_US
dc.identifier.isiWOS:000171327400012-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridFung, ML=7101955092en_US
dc.identifier.scopusauthoridDong, X=55184171400en_US

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