Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/13597
Full metadata record
DC FieldValueLanguage
dc.contributor.authorBurazin, T Cen
dc.contributor.authorGundlach, Andrew Len
dc.date.accessioned2015-05-16T03:28:55Z
dc.date.available2015-05-16T03:28:55Z
dc.date.issued1998-04-01en
dc.identifier.citationBrain Research. Molecular Brain Research; 55(2): 331-6en
dc.identifier.govdoc9582449en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/13597en
dc.description.abstractGlial cell line-derived neurotrophic factor (GDNF), a powerful trophic factor for developing, and injured adult motor neurons, has recently been shown to mediate its physiological effects via a multi-component receptor system comprising the GDNFR-alpha binding protein and the c-ret receptor tyrosine kinase. Using in situ hybridization histochemistry this study investigated whether adult motor neurons express mRNAs encoding GDNFR-alpha and c-ret, and explored possible time-dependent changes in these mRNA species following facial nerve resection and crush injury. Levels of mRNA for the signaling component of the GDNF receptor, c-ret, were increased approximately 1.4-fold in the ipsilateral facial nucleus, 1 and 3 days after unilateral facial nerve crush and resection, but returned to contralateral levels by 7-21 days. GDNFR-alpha mRNA was increased from 2 to 3-fold in the facial nucleus at 1 and 3 days after facial nerve crush and to similar, but more sustained (up to 21 days), levels after resection. In contrast, GDNF mRNA was not detectable in normal or injured facial motor neurons. The gradual return of c-ret and GDNFR-alpha mRNAs to control levels 21 days after facial nerve crush, parallels the axonal regeneration process, while nerve damage by resection has more severe consequences compared to nerve crush, reflected by the prolonged time course of increased GDNFR-alpha mRNA, similar to markers such as the NGF-receptor, galanin and GAP-43. These findings confirm the importance of GDNF trophic/signaling systems after nerve injury and suggest the potential for broad biological and therapeutic actions of GDNF or related factors in the CNS, particularly on damaged motor neurons.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherBrainen
dc.subject.otherDrosophila Proteinsen
dc.subject.otherFacial Nerve.metabolism.physiologyen
dc.subject.otherGlial Cell Line-Derived Neurotrophic Factor Receptorsen
dc.subject.otherMaleen
dc.subject.otherMotor Neurons.metabolism.physiologyen
dc.subject.otherNerve Crushen
dc.subject.otherNeuroglia.metabolismen
dc.subject.otherProto-Oncogene Proteins.biosynthesis.geneticsen
dc.subject.otherProto-Oncogene Proteins c-reten
dc.subject.otherRNA, Messenger.biosynthesisen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherReceptor Protein-Tyrosine Kinases.biosynthesis.geneticsen
dc.subject.otherUp-Regulation.geneticsen
dc.titleUp-regulation of GDNFR-alpha and c-ret mRNA in facial motor neurons following facial nerve injury in the rat.en
dc.typeJournal Articleen
dc.identifier.journaltitleBrain Research. Molecular Brain Researchen
dc.identifier.affiliationThe University of Melbourne, Clinical Pharmacology and Therapeutics Unit, Department of Medicine, Austin and Repatriation Medical Centre, Heidelberg, Victoria 3084, Australiaen
dc.description.pages331-6en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/9582449en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
Appears in Collections:Journal articles
Show simple item record

Page view(s)

4
checked on Mar 28, 2024

Google ScholarTM

Check


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.