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Article: Neuropeptide Y and its receptor analogs differentially modulate the immunoreactivity for neuronal or endothelial nitric oxide synthase in the rat brain following focal ischemia with reperfusion

TitleNeuropeptide Y and its receptor analogs differentially modulate the immunoreactivity for neuronal or endothelial nitric oxide synthase in the rat brain following focal ischemia with reperfusion
Authors
Issue Date2005
PublisherSpringer Verlag Dordrecht. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=1021-7770
Citation
Journal Of Biomedical Science, 2005, v. 12 n. 2, p. 267-278 How to Cite?
AbstractAn intracerebroventricular (icv) injection of neuropeptide Y (NPY) or [Leu31, Pro34]-NPY (non-Y2 receptor agonist) given during middle cerebral artery occlusion (MCAO) increases the infarct volume and nitric oxide (NO) overproduction in the rat brain. An icv injection of NPY3-36 (non-Y1 receptor agonist) has no effects, while BIBP3226 (selective Y1 receptor antagonist) reduces the infarct volume and NO overproduction. This study examined the effects of NPY or its receptor analog on the immunoreactivity (ir) for three isoforms of NO synthase (NOS) following 1∈h of MCAO and 3∈h of reperfusion. Focal ischemia/reperfusion led to increased ir for neuronal NOS (nNOS) within the ipsilateral caudate putamen and insular cortex. NPY or [Leu31, Pro34]-NPY enhanced but BIBP3226 suppressed such increase in the nNOS-ir. Focal ischemia/reperfusion also led to an ipsilateral increase in extent and/or intensity of the ir for endothelial NOS (eNOS) in the caudate putamen and/or parietal cortex. NPY or [Leu31, Pro 34]-NPY suppressed but BIBP3226 enhanced such change in the eNOS-ir. NPY3-36 did not consistently influence the nNOS-ir or eNOS-ir following MCAO. Specific ir for inducible NOS was undetectable. These opposing effects of NPY-Y1 receptor activation or inhibition on nNOS and eNOS may lead to harmful or beneficial consequences following ischemia/reperfusion. © 2005 National Science Council.
Persistent Identifierhttp://hdl.handle.net/10722/77464
ISSN
2015 Impact Factor: 2.935
2015 SCImago Journal Rankings: 1.280
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShao, HCen_HK
dc.contributor.authorCheung, RTFen_HK
dc.date.accessioned2010-09-06T07:32:11Z-
dc.date.available2010-09-06T07:32:11Z-
dc.date.issued2005en_HK
dc.identifier.citationJournal Of Biomedical Science, 2005, v. 12 n. 2, p. 267-278en_HK
dc.identifier.issn1021-7770en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77464-
dc.description.abstractAn intracerebroventricular (icv) injection of neuropeptide Y (NPY) or [Leu31, Pro34]-NPY (non-Y2 receptor agonist) given during middle cerebral artery occlusion (MCAO) increases the infarct volume and nitric oxide (NO) overproduction in the rat brain. An icv injection of NPY3-36 (non-Y1 receptor agonist) has no effects, while BIBP3226 (selective Y1 receptor antagonist) reduces the infarct volume and NO overproduction. This study examined the effects of NPY or its receptor analog on the immunoreactivity (ir) for three isoforms of NO synthase (NOS) following 1∈h of MCAO and 3∈h of reperfusion. Focal ischemia/reperfusion led to increased ir for neuronal NOS (nNOS) within the ipsilateral caudate putamen and insular cortex. NPY or [Leu31, Pro34]-NPY enhanced but BIBP3226 suppressed such increase in the nNOS-ir. Focal ischemia/reperfusion also led to an ipsilateral increase in extent and/or intensity of the ir for endothelial NOS (eNOS) in the caudate putamen and/or parietal cortex. NPY or [Leu31, Pro 34]-NPY suppressed but BIBP3226 enhanced such change in the eNOS-ir. NPY3-36 did not consistently influence the nNOS-ir or eNOS-ir following MCAO. Specific ir for inducible NOS was undetectable. These opposing effects of NPY-Y1 receptor activation or inhibition on nNOS and eNOS may lead to harmful or beneficial consequences following ischemia/reperfusion. © 2005 National Science Council.en_HK
dc.languageengen_HK
dc.publisherSpringer Verlag Dordrecht. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=1021-7770en_HK
dc.relation.ispartofJournal of Biomedical Scienceen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAnti-Anxiety Agents - pharmacologyen_HK
dc.subject.meshArginine - analogs & derivatives - pharmacologyen_HK
dc.subject.meshBrain - metabolism - pathologyen_HK
dc.subject.meshBrain Ischemia - pathologyen_HK
dc.subject.meshCerebral Arteries - pathologyen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshMaleen_HK
dc.subject.meshNeurons - metabolismen_HK
dc.subject.meshNeuropeptide Y - metabolism - pharmacology - physiologyen_HK
dc.subject.meshNitric Oxide - metabolismen_HK
dc.subject.meshNitric Oxide Synthase - metabolismen_HK
dc.subject.meshNitric Oxide Synthase Type IIIen_HK
dc.subject.meshProtein Isoformsen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshReceptors, Neuropeptide Y - metabolism - physiologyen_HK
dc.subject.meshReperfusion Injuryen_HK
dc.subject.meshTemperatureen_HK
dc.subject.meshTime Factorsen_HK
dc.titleNeuropeptide Y and its receptor analogs differentially modulate the immunoreactivity for neuronal or endothelial nitric oxide synthase in the rat brain following focal ischemia with reperfusionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1021-7770&volume=12&spage=267&epage=278&date=2005&atitle=Neuropeptide+Y+and+its+receptor+analogs+differentially+modulate+the+immunoreactivity+for+neuronal+or+endothelial+nitric+oxide+synthase+in+the+rat+brain+following+focal+ischemia+with+reperfusionen_HK
dc.identifier.emailCheung, RTF:rtcheung@hku.hken_HK
dc.identifier.authorityCheung, RTF=rp00434en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s11373-005-1359-yen_HK
dc.identifier.pmid15942706-
dc.identifier.scopuseid_2-s2.0-21244497681en_HK
dc.identifier.hkuros99207en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-21244497681&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume12en_HK
dc.identifier.issue2en_HK
dc.identifier.spage267en_HK
dc.identifier.epage278en_HK
dc.identifier.isiWOS:000230594700002-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridShao, HC=8601305500en_HK
dc.identifier.scopusauthoridCheung, RTF=7202397498en_HK

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