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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
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TitleGlial and axonal responses in areas of Wallerian degeneration of the corticospinal and dorsal ascending tracts after spinal cord dorsal funiculotomy
 
AuthorsWang, L2 3
Hu, B2
Wong, WM2
Lu, P3
Wu, W2
Xu, XM3 1
 
Issue Date2009
 
PublisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/NEU
 
CitationNeuropathology, 2009, v. 29 n. 3, p. 230-241 [How to Cite?]
DOI: http://dx.doi.org/10.1111/j.1440-1789.2008.00969.x
 
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.
 
ISSN0919-6544
2013 Impact Factor: 1.796
 
DOIhttp://dx.doi.org/10.1111/j.1440-1789.2008.00969.x
 
ISI Accession Number IDWOS:000266072900003
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).

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorWang, L
 
dc.contributor.authorHu, B
 
dc.contributor.authorWong, WM
 
dc.contributor.authorLu, P
 
dc.contributor.authorWu, W
 
dc.contributor.authorXu, XM
 
dc.date.accessioned2010-05-31T03:25:27Z
 
dc.date.available2010-05-31T03:25:27Z
 
dc.date.issued2009
 
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.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationNeuropathology, 2009, v. 29 n. 3, p. 230-241 [How to Cite?]
DOI: http://dx.doi.org/10.1111/j.1440-1789.2008.00969.x
 
dc.identifier.citeulike4536740
 
dc.identifier.doihttp://dx.doi.org/10.1111/j.1440-1789.2008.00969.x
 
dc.identifier.epage241
 
dc.identifier.hkuros163964
 
dc.identifier.isiWOS:000266072900003
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).

 
dc.identifier.issn0919-6544
2013 Impact Factor: 1.796
 
dc.identifier.issue3
 
dc.identifier.openurl
 
dc.identifier.pmid18992013
 
dc.identifier.scopuseid_2-s2.0-65649151402
 
dc.identifier.spage230
 
dc.identifier.urihttp://hdl.handle.net/10722/58187
 
dc.identifier.volume29
 
dc.languageeng
 
dc.publisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/NEU
 
dc.publisher.placeAustralia
 
dc.relation.ispartofNeuropathology
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAnimals
 
dc.subject.meshAstrocytes - physiology - ultrastructure
 
dc.subject.meshAxons - physiology - ultrastructure
 
dc.subject.meshBasic Helix-Loop-Helix Transcription Factors - metabolism
 
dc.subject.meshFemale
 
dc.subject.meshGlial Fibrillary Acidic Protein - metabolism
 
dc.subject.meshMacrophages - physiology - ultrastructure
 
dc.subject.meshMicroglia - physiology - ultrastructure
 
dc.subject.meshMyelin Sheath - physiology - ultrastructure
 
dc.subject.meshNerve Tissue Proteins - metabolism
 
dc.subject.meshNeural Pathways - physiopathology - ultrastructure
 
dc.subject.meshNeuroglia - physiology - ultrastructure
 
dc.subject.meshPyramidal Tracts - physiopathology - ultrastructure
 
dc.subject.meshRats
 
dc.subject.meshRats, Sprague-Dawley
 
dc.subject.meshSpinal Cord Injuries - pathology - physiopathology
 
dc.subject.meshThoracic Vertebrae
 
dc.subject.meshTime Factors
 
dc.subject.meshWallerian Degeneration - physiopathology
 
dc.titleGlial and axonal responses in areas of Wallerian degeneration of the corticospinal and dorsal ascending tracts after spinal cord dorsal funiculotomy
 
dc.typeArticle
 
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Author Affiliations
  1. Indiana University School of Medicine Indianapolis
  2. The University of Hong Kong
  3. Shanghai Jiaotong University