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Article: Expression and role of low-affinity nerve growth factor receptor (p75) in spinal motor neurons of aged rats following axonal injury

TitleExpression and role of low-affinity nerve growth factor receptor (p75) in spinal motor neurons of aged rats following axonal injury
Authors
KeywordsAged spinal motor neuron
Avulsion
Axotomy
Immunocytochemistry
p75
Issue Date2003
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/DNE
Citation
Developmental Neuroscience, 2003, v. 25 n. 1, p. 65-71 How to Cite?
AbstractExpression of low-affinity nerve growth factor receptor (p75) and its regulation in spinal motor neurons of aged rats following axonal injury were investigated by immunocytochemical staining with antibody against p75. Under normal conditions, approximately 60% of spinal motor neurons expressed p75 in aged rats whereas no p75 expression was observed in spinal motor neurons of young adult rats. We examined the effects of spinal motor neuron injury on aged rats by two approaches, i.e. distal axotomy and spinal nerve root avulsion. A 20% increase in the number of p75-positive motor neurons was observed in aged rats 2 weeks after distal axotomy after which it returned to normal by 8 weeks post-injury and remained constant. Following root avulsion, a transient and slight up-regulation of p75 expression was observed in injured motor neurons. The number of p75-positive motor neurons decreased quickly to below normal levels 1 week after lesion and progressively declined with time post-injury, 40% by 2 weeks, 33% by 4 weeks, 23% by 8 weeks, and 5.8% by 12 weeks compared with the normal controls. This study demonstrates that p75 is re-expressed in aged spinal motor neurons. Following axonal injury in aged rats, up-regulation of p75 seems to coincide with the survival of injured motor neurons. Potential roles of re-expression of p75 in aged motor neurons are discussed. Copyright © 2003 S. Karger AG, Basel.
Persistent Identifierhttp://hdl.handle.net/10722/67775
ISSN
2023 Impact Factor: 2.3
2023 SCImago Journal Rankings: 0.954
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXie, Yen_HK
dc.contributor.authorYao, Zen_HK
dc.contributor.authorChai, Hen_HK
dc.contributor.authorWong, WMen_HK
dc.contributor.authorWu, Wen_HK
dc.date.accessioned2010-09-06T05:58:08Z-
dc.date.available2010-09-06T05:58:08Z-
dc.date.issued2003en_HK
dc.identifier.citationDevelopmental Neuroscience, 2003, v. 25 n. 1, p. 65-71en_HK
dc.identifier.issn0378-5866en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67775-
dc.description.abstractExpression of low-affinity nerve growth factor receptor (p75) and its regulation in spinal motor neurons of aged rats following axonal injury were investigated by immunocytochemical staining with antibody against p75. Under normal conditions, approximately 60% of spinal motor neurons expressed p75 in aged rats whereas no p75 expression was observed in spinal motor neurons of young adult rats. We examined the effects of spinal motor neuron injury on aged rats by two approaches, i.e. distal axotomy and spinal nerve root avulsion. A 20% increase in the number of p75-positive motor neurons was observed in aged rats 2 weeks after distal axotomy after which it returned to normal by 8 weeks post-injury and remained constant. Following root avulsion, a transient and slight up-regulation of p75 expression was observed in injured motor neurons. The number of p75-positive motor neurons decreased quickly to below normal levels 1 week after lesion and progressively declined with time post-injury, 40% by 2 weeks, 33% by 4 weeks, 23% by 8 weeks, and 5.8% by 12 weeks compared with the normal controls. This study demonstrates that p75 is re-expressed in aged spinal motor neurons. Following axonal injury in aged rats, up-regulation of p75 seems to coincide with the survival of injured motor neurons. Potential roles of re-expression of p75 in aged motor neurons are discussed. Copyright © 2003 S. Karger AG, Basel.en_HK
dc.languageengen_HK
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/DNEen_HK
dc.relation.ispartofDevelopmental Neuroscienceen_HK
dc.rightsDevelopmental Neuroscience. Copyright © S Karger AG.en_HK
dc.subjectAged spinal motor neuron-
dc.subjectAvulsion-
dc.subjectAxotomy-
dc.subjectImmunocytochemistry-
dc.subjectp75-
dc.subject.meshAging - metabolismen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAxotomyen_HK
dc.subject.meshBinding, Competitiveen_HK
dc.subject.meshCell Counten_HK
dc.subject.meshCell Survivalen_HK
dc.subject.meshDiffuse Axonal Injury - metabolism - pathology - physiopathologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMotor Neurons - metabolism - pathologyen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshReceptor, Nerve Growth Factoren_HK
dc.subject.meshReceptors, Nerve Growth Factor - metabolismen_HK
dc.subject.meshSpinal Cord - metabolismen_HK
dc.titleExpression and role of low-affinity nerve growth factor receptor (p75) in spinal motor neurons of aged rats following axonal injuryen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0378-5866&volume=25&spage=65&epage=71&date=2003&atitle=Expression+and+role+of+low-affinity+nerve+growth+factor+receptor+(p75)+in+spinal+motor+neurons+of+aged+rats+following+axonal+injuryen_HK
dc.identifier.emailWu, W:wtwu@hkucc.hku.hken_HK
dc.identifier.authorityWu, W=rp00419en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1159/000071469en_HK
dc.identifier.pmid12876432en_HK
dc.identifier.scopuseid_2-s2.0-0043166787en_HK
dc.identifier.hkuros85078en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0043166787&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume25en_HK
dc.identifier.issue1en_HK
dc.identifier.spage65en_HK
dc.identifier.epage71en_HK
dc.identifier.isiWOS:000184494800008-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridXie, Y=7403958873en_HK
dc.identifier.scopusauthoridYao, Z=7401467890en_HK
dc.identifier.scopusauthoridChai, H=35918658800en_HK
dc.identifier.scopusauthoridWong, WM=7403972413en_HK
dc.identifier.scopusauthoridWu, W=7407081122en_HK
dc.identifier.issnl0378-5866-

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