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Article: Inflammatory response associated with axonal injury to spinal motoneurons in newborn rats

TitleInflammatory response associated with axonal injury to spinal motoneurons in newborn rats
Authors
KeywordsAvulsion
Axotomy
Microglia
Neuronal death
Phagocytes
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. 72-78 How to Cite?
AbstractAxonal injury in peripheral nerve results in massive motoneuron loss during development. The purpose of this study was to examine the response of phagocytic populations (brain macrophages, BMOs, versus microglia) after different types of axonal lesions (distal axotomy or avulsion) in newborn rats. The morphology, spatial location and activation state of these inflammatory cells were observed. Following spinal root avulsion, BMOs were signaled rapidly and specifically to the location of dying motoneurons in the spinal cord. A large number of BMOs were observed around the avulsed motoneurons on the lesioned side of the spinal cord 1 day following the lesion. These BMOs were large, round, and intensely stained by both antibodies against ED1 and OX-42. The number of BMOs decreased by 3 days and disappeared by 5 days after injury. At the same time, reactive microglia appeared in the lesioned area and rapidly reached the peak level by the 5th day following avulsion. These reactive microglia were medium in size with retracted cellular processes and were also intensely stained by both ED1 and OX-42 antibodies. The number and staining intensity of reactive microglia declined sharply by day 7 after the lesion. In contrast, after distal axotomy only microglia but not BMOs were observed in the lesioned area. These microglial cells were small in size with long and fine-branched processes. They were ED1-negative but OX-42-positive. Copyright © 2003 S. Karger AG, Basel.
Persistent Identifierhttp://hdl.handle.net/10722/67504
ISSN
2021 Impact Factor: 3.421
2020 SCImago Journal Rankings: 0.893
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYuan, Qen_HK
dc.contributor.authorXie, Yen_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorWu, Wen_HK
dc.date.accessioned2010-09-06T05:55:43Z-
dc.date.available2010-09-06T05:55:43Z-
dc.date.issued2003en_HK
dc.identifier.citationDevelopmental Neuroscience, 2003, v. 25 n. 1, p. 72-78en_HK
dc.identifier.issn0378-5866en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67504-
dc.description.abstractAxonal injury in peripheral nerve results in massive motoneuron loss during development. The purpose of this study was to examine the response of phagocytic populations (brain macrophages, BMOs, versus microglia) after different types of axonal lesions (distal axotomy or avulsion) in newborn rats. The morphology, spatial location and activation state of these inflammatory cells were observed. Following spinal root avulsion, BMOs were signaled rapidly and specifically to the location of dying motoneurons in the spinal cord. A large number of BMOs were observed around the avulsed motoneurons on the lesioned side of the spinal cord 1 day following the lesion. These BMOs were large, round, and intensely stained by both antibodies against ED1 and OX-42. The number of BMOs decreased by 3 days and disappeared by 5 days after injury. At the same time, reactive microglia appeared in the lesioned area and rapidly reached the peak level by the 5th day following avulsion. These reactive microglia were medium in size with retracted cellular processes and were also intensely stained by both ED1 and OX-42 antibodies. The number and staining intensity of reactive microglia declined sharply by day 7 after the lesion. In contrast, after distal axotomy only microglia but not BMOs were observed in the lesioned area. These microglial cells were small in size with long and fine-branched processes. They were ED1-negative but OX-42-positive. 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.subjectAvulsion-
dc.subjectAxotomy-
dc.subjectMicroglia-
dc.subjectNeuronal death-
dc.subjectPhagocytes-
dc.subject.meshAnimalsen_HK
dc.subject.meshAnimals, Newbornen_HK
dc.subject.meshBrain - pathologyen_HK
dc.subject.meshDiffuse Axonal Injury - complicationsen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshMacrophages - pathologyen_HK
dc.subject.meshMicroglia - pathologyen_HK
dc.subject.meshMotor Neurons - pathologyen_HK
dc.subject.meshMyelitis - etiology - pathologyen_HK
dc.subject.meshRadiculopathy - complicationsen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshSpinal Cord - pathologyen_HK
dc.titleInflammatory response associated with axonal injury to spinal motoneurons in newborn ratsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0378-5866&volume=25&spage=72&epage=78&date=2003&atitle=Inflammatory+response+associated+with+axonal+injury+to+spinal+motoneurons+in+newborn+ratsen_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.doi10.1159/000071470en_HK
dc.identifier.pmid12876433-
dc.identifier.scopuseid_2-s2.0-0043166781en_HK
dc.identifier.hkuros85077en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0043166781&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume25en_HK
dc.identifier.issue1en_HK
dc.identifier.spage72en_HK
dc.identifier.epage78en_HK
dc.identifier.isiWOS:000184494800009-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridYuan, Q=7202814773en_HK
dc.identifier.scopusauthoridXie, Y=7403958873en_HK
dc.identifier.scopusauthoridSo, KF=34668391300en_HK
dc.identifier.scopusauthoridWu, W=7407081122en_HK
dc.identifier.issnl0378-5866-

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