File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: The potential role of nitric oxide synthase in survival and regeneration of magnocellular neurons of hypothalamo-neurohypophyseal system

TitleThe potential role of nitric oxide synthase in survival and regeneration of magnocellular neurons of hypothalamo-neurohypophyseal system
Authors
KeywordsAxonal injury
Endocrine hypothalamus
Neuronal plasticity
Nitric oxide
Issue Date2009
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0364-3190
Citation
Neurochemical Research, 2009, v. 34 n. 11, p. 1907-1913 How to Cite?
AbstractPrevious investigations from this laboratory have demonstrated that hypophysectomy induces up-regulation of neuronal nitric oxide synthase (nNOS) in magnocellular neurons of the mammalian hypothalamo-neurohypophyseal system (HNS). Accompanied by this upregulation of nNOS, both neuronal regeneration and degeneration are also observed in this system following hypophysectomy. The specific aim of this study was to determine the potential role of nNOS upregulation in neuronal survival and regeneration after hypophysectomy in the adult Sprague-Dawley (SD) rat by using a competitive nitric oxide synthase blocker, N(G)-nitrol-l-arginine methyl ester (l-NAME). We found that l-NAME treatment effectively blocked the regeneration of magnocellular neurons of the rodent hypothalamus as observed in the lumen of the third cerebral ventricle following hypophysectomy. However, l-NAME had no effect on the survival of magnocellular neurons in the supraoptic (SON) and paraventricular (PVN) nuclei after hypophysectomy. These results suggest that the induced increase of nNOS expression enhance the regenerative ability of magnocellular neurons of the HNS following hypophysectomy. © 2009 Springer Science+Business Media, LLC.
Persistent Identifierhttp://hdl.handle.net/10722/58193
ISSN
2021 Impact Factor: 4.414
2020 SCImago Journal Rankings: 1.102
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYuan, Qen_HK
dc.contributor.authorScott, DEen_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorLin, Zen_HK
dc.contributor.authorWu, Wen_HK
dc.date.accessioned2010-05-31T03:25:34Z-
dc.date.available2010-05-31T03:25:34Z-
dc.date.issued2009en_HK
dc.identifier.citationNeurochemical Research, 2009, v. 34 n. 11, p. 1907-1913en_HK
dc.identifier.issn0364-3190en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58193-
dc.description.abstractPrevious investigations from this laboratory have demonstrated that hypophysectomy induces up-regulation of neuronal nitric oxide synthase (nNOS) in magnocellular neurons of the mammalian hypothalamo-neurohypophyseal system (HNS). Accompanied by this upregulation of nNOS, both neuronal regeneration and degeneration are also observed in this system following hypophysectomy. The specific aim of this study was to determine the potential role of nNOS upregulation in neuronal survival and regeneration after hypophysectomy in the adult Sprague-Dawley (SD) rat by using a competitive nitric oxide synthase blocker, N(G)-nitrol-l-arginine methyl ester (l-NAME). We found that l-NAME treatment effectively blocked the regeneration of magnocellular neurons of the rodent hypothalamus as observed in the lumen of the third cerebral ventricle following hypophysectomy. However, l-NAME had no effect on the survival of magnocellular neurons in the supraoptic (SON) and paraventricular (PVN) nuclei after hypophysectomy. These results suggest that the induced increase of nNOS expression enhance the regenerative ability of magnocellular neurons of the HNS following hypophysectomy. © 2009 Springer Science+Business Media, LLC.en_HK
dc.languageengen_HK
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0364-3190en_HK
dc.relation.ispartofNeurochemical Researchen_HK
dc.subjectAxonal injury-
dc.subjectEndocrine hypothalamus-
dc.subjectNeuronal plasticity-
dc.subjectNitric oxide-
dc.subject.meshAnimalsen_HK
dc.subject.meshCell Survivalen_HK
dc.subject.meshHypophysectomyen_HK
dc.subject.meshHypothalamo-Hypophyseal System - cytology - drug effectsen_HK
dc.subject.meshMaleen_HK
dc.subject.meshNG-Nitroarginine Methyl Ester - pharmacologyen_HK
dc.subject.meshNeuronal Plasticityen_HK
dc.subject.meshNeurons - cytology - physiologyen_HK
dc.subject.meshNitric Oxide Synthase Type I - antagonists & inhibitors - physiologyen_HK
dc.subject.meshParaventricular Hypothalamic Nucleus - cytology - drug effectsen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshRegenerationen_HK
dc.subject.meshSupraoptic Nucleus - cytology - drug effectsen_HK
dc.titleThe potential role of nitric oxide synthase in survival and regeneration of magnocellular neurons of hypothalamo-neurohypophyseal systemen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0364-3190&volume=34&issue=11&spage=1907&epage=1913&date=2009&atitle=The+Potential+Role+of+Nitric+Oxide+Synthase+in+Survival+and+Regeneration+of+Magnocellular+Neurons+of+Hypothalamo-Neurohypophyseal+System.en_HK
dc.identifier.emailSo, KF:hrmaskf@hkucc.hku.hken_HK
dc.identifier.emailWu, W:wtwu@hkucc.hku.hken_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.identifier.authorityWu, W=rp00419en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s11064-009-9965-0en_HK
dc.identifier.pmid19381805-
dc.identifier.scopuseid_2-s2.0-70349606148en_HK
dc.identifier.hkuros163983en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-70349606148&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume34en_HK
dc.identifier.issue11en_HK
dc.identifier.spage1907en_HK
dc.identifier.epage1913en_HK
dc.identifier.isiWOS:000269914400003-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYuan, Q=7202814773en_HK
dc.identifier.scopusauthoridScott, DE=40262460100en_HK
dc.identifier.scopusauthoridSo, KF=34668391300en_HK
dc.identifier.scopusauthoridLin, Z=26433004200en_HK
dc.identifier.scopusauthoridWu, W=7407081122en_HK
dc.identifier.citeulike4383100-
dc.identifier.issnl0364-3190-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats