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Article: Glial and axonal responses in areas of Wallerian degeneration of the corticospinal and dorsal ascending tracts after spinal cord dorsal funiculotomy

TitleGlial and axonal responses in areas of Wallerian degeneration of the corticospinal and dorsal ascending tracts after spinal cord dorsal funiculotomy
Authors
Issue Date2009
PublisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/NEU
Citation
Neuropathology, 2009, v. 29 n. 3, p. 230-241 How to Cite?
AbstractWallerian degeneration (WD), composed of the breakdown and phagocytosis of damaged axons and their myelin sheaths distal to the injury, is a major sequela of spinal cord injury (SCI). To understand the microenvironment within WD that may affect repair following SCI, we investigated the fate of major glial types and axons in this region following acute (1 h), subacute (10 days), and chronic (30 days) dorsal funiculotomy at the eighth thoracic (T8) level. This lesion induces a confined WD in two distinct functional pathways, that is, the corticospinal tract (CST) and dorsal ascending tract (DAT) in opposite directions. Here we report that astrocytes, reactive microglia and macrophages were all significantly increased in areas of WD in both the CST and DAT at subacute and chronic stages compared to the sham-operated or acute stage. While the level of GFAP + astrocytes remained stable after the subacute stage, the number of OX-42 + microglia and ED-1 + macrophages markedly decreased at the chronic stage. Interestingly, a mild but significant increase in ED-1 + macrophages was also found in the intact fiber tracts 3 mm proximal to the injury at the chronic stage, coinciding with axonal dieback observed at that level. Axons distal to the injury experienced a continued and prolonged degeneration in both fiber tracts. Finally, although a significant decrease of Olig2 + oligodendrocyte lineage (OL) cells was found in areas of WD, the presence of these cells at the chronic stage indicates that they are available for endogenous repair. Taken together, our data have provided spatiotemporal evidence for the dynamic pathogenic changes of major cellular components in areas of WD remote to an SCI. Information obtained in this study should be useful for designing experiments aimed at modifying this region to accommodate endogenous or exogenous repair following SCI. © 2008 Japanese Society of Neuropathology.
Persistent Identifierhttp://hdl.handle.net/10722/58187
ISSN
2014 Impact Factor: 1.651
2014 SCImago Journal Rankings: 0.645
ISI Accession Number ID
Funding AgencyGrant Number
Major State Basic Research Development Program of China2003CB515302
University of Hong Kong
Research Grant Council of Hong Kong
NIH NINDSNS36350
NS52290
NS50253
Daniel Heumann Fund for Spinal Cord Research (XMX)
Funding Information:

This study was supported by Major State Basic Research Development Program of China (973 Project; 2003CB515302) (PL), University of Hong Kong and the Research Grant Council of Hong Kong (WW) and NIH NINDS (NS36350, NS52290, NS50253) and the Daniel Heumann Fund for Spinal Cord Research (XMX).

References

 

DC FieldValueLanguage
dc.contributor.authorWang, Len_HK
dc.contributor.authorHu, Ben_HK
dc.contributor.authorWong, WMen_HK
dc.contributor.authorLu, Pen_HK
dc.contributor.authorWu, Wen_HK
dc.contributor.authorXu, XMen_HK
dc.date.accessioned2010-05-31T03:25:27Z-
dc.date.available2010-05-31T03:25:27Z-
dc.date.issued2009en_HK
dc.identifier.citationNeuropathology, 2009, v. 29 n. 3, p. 230-241en_HK
dc.identifier.issn0919-6544en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58187-
dc.description.abstractWallerian degeneration (WD), composed of the breakdown and phagocytosis of damaged axons and their myelin sheaths distal to the injury, is a major sequela of spinal cord injury (SCI). To understand the microenvironment within WD that may affect repair following SCI, we investigated the fate of major glial types and axons in this region following acute (1 h), subacute (10 days), and chronic (30 days) dorsal funiculotomy at the eighth thoracic (T8) level. This lesion induces a confined WD in two distinct functional pathways, that is, the corticospinal tract (CST) and dorsal ascending tract (DAT) in opposite directions. Here we report that astrocytes, reactive microglia and macrophages were all significantly increased in areas of WD in both the CST and DAT at subacute and chronic stages compared to the sham-operated or acute stage. While the level of GFAP + astrocytes remained stable after the subacute stage, the number of OX-42 + microglia and ED-1 + macrophages markedly decreased at the chronic stage. Interestingly, a mild but significant increase in ED-1 + macrophages was also found in the intact fiber tracts 3 mm proximal to the injury at the chronic stage, coinciding with axonal dieback observed at that level. Axons distal to the injury experienced a continued and prolonged degeneration in both fiber tracts. Finally, although a significant decrease of Olig2 + oligodendrocyte lineage (OL) cells was found in areas of WD, the presence of these cells at the chronic stage indicates that they are available for endogenous repair. Taken together, our data have provided spatiotemporal evidence for the dynamic pathogenic changes of major cellular components in areas of WD remote to an SCI. Information obtained in this study should be useful for designing experiments aimed at modifying this region to accommodate endogenous or exogenous repair following SCI. © 2008 Japanese Society of Neuropathology.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/NEUen_HK
dc.relation.ispartofNeuropathologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAstrocytes - physiology - ultrastructureen_HK
dc.subject.meshAxons - physiology - ultrastructureen_HK
dc.subject.meshBasic Helix-Loop-Helix Transcription Factors - metabolismen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGlial Fibrillary Acidic Protein - metabolismen_HK
dc.subject.meshMacrophages - physiology - ultrastructureen_HK
dc.subject.meshMicroglia - physiology - ultrastructureen_HK
dc.subject.meshMyelin Sheath - physiology - ultrastructureen_HK
dc.subject.meshNerve Tissue Proteins - metabolismen_HK
dc.subject.meshNeural Pathways - physiopathology - ultrastructureen_HK
dc.subject.meshNeuroglia - physiology - ultrastructureen_HK
dc.subject.meshPyramidal Tracts - physiopathology - ultrastructureen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshSpinal Cord Injuries - pathology - physiopathologyen_HK
dc.subject.meshThoracic Vertebraeen_HK
dc.subject.meshTime Factorsen_HK
dc.subject.meshWallerian Degeneration - physiopathologyen_HK
dc.titleGlial and axonal responses in areas of Wallerian degeneration of the corticospinal and dorsal ascending tracts after spinal cord dorsal funiculotomyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0919-6544&volume=29&issue=3&spage=230&epage=241&date=2008&atitle=Glial+and+axonal+responses+in+areas+of+Wallerian+degeneration+of+the+corticospinal+and+dorsal+ascending+tracts+after+spinal+cord+dorsal+funiculotomyen_HK
dc.identifier.emailWu, W:wtwu@hkucc.hku.hken_HK
dc.identifier.authorityWu, W=rp00419en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1440-1789.2008.00969.xen_HK
dc.identifier.pmid18992013en_HK
dc.identifier.scopuseid_2-s2.0-65649151402en_HK
dc.identifier.hkuros163964en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-65649151402&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume29en_HK
dc.identifier.issue3en_HK
dc.identifier.spage230en_HK
dc.identifier.epage241en_HK
dc.identifier.isiWOS:000266072900003-
dc.publisher.placeAustraliaen_HK
dc.identifier.scopusauthoridWang, L=36851751100en_HK
dc.identifier.scopusauthoridHu, B=35733928400en_HK
dc.identifier.scopusauthoridWong, WM=7403972413en_HK
dc.identifier.scopusauthoridLu, P=7402292929en_HK
dc.identifier.scopusauthoridWu, W=7407081122en_HK
dc.identifier.scopusauthoridXu, XM=7405298291en_HK
dc.identifier.citeulike4536740-

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