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Article: Axonal regeneration of Clarke's neurons beyond the spinal cord injury scar after treatment with chondroitinase ABC

TitleAxonal regeneration of Clarke's neurons beyond the spinal cord injury scar after treatment with chondroitinase ABC
Authors
KeywordsAxotomy
Chondroitin sulfate
Proteoglycans
Regrowth
Spinal cord
Traumatic injury
Issue Date2003
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexnr
Citation
Experimental Neurology, 2003, v. 182 n. 1, p. 160-168 How to Cite?
AbstractWe have previously demonstrated that enzymatic digestion of chondroitin sulfate proteoglycan (CSPG) at the scar promotes the axonal regrowth of Clarke's nucleus (CN) neurons into an implanted peripheral nerve graft after hemisection of the spinal cord. The present study examined whether degradation of CSPG using chondroitinase ABC promoted the regeneration of CN neurons through the scar into the rostral spinal cord in neonatal and adult rats. Following hemisection of the spinal cord at T11, either vehicle or chondroitinase ABC was applied onto the lesion site. The postoperative survival periods were 2 and 4 weeks. The regenerated CN neurons were retrogradely labeled by Fluoro-Gold injected at spinal cord level C7. In the sham group, there was no regeneration of injured CN neurons in both neonatal and adult rats. Treatment with 2.5 unit/ml chondroitinase ABC in neonates resulted in 11.8 and 8.3% of the injured CN neurons regenerated into the rostral spinal cord at 2 and 4 weeks, respectively. In adults, 9.4 and 12.3%, at 2 and 4 weeks, respectively, of the injured CN neurons regenerated their axons to the rostral spinal cord. The immunoreactivity for the carbohydrate epitope of CSPG was dramatically decreased around the lesion site after treatment with chondroitinase ABC compared to sham control in both neonatal and adult animals. Our results show that axonal regeneration in the spinal cord can be promoted by degradation of CSPG with chondroitinase ABC. This result further suggests that CSPG is inhibitory to the regeneration of neurons in the spinal cord after traumatic injury. © 2003 Elsevier Science (USA). All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67950
ISSN
2015 Impact Factor: 4.657
2015 SCImago Journal Rankings: 2.427
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYick, LWen_HK
dc.contributor.authorCheung, PTen_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorWu, Wen_HK
dc.date.accessioned2010-09-06T05:59:44Z-
dc.date.available2010-09-06T05:59:44Z-
dc.date.issued2003en_HK
dc.identifier.citationExperimental Neurology, 2003, v. 182 n. 1, p. 160-168en_HK
dc.identifier.issn0014-4886en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67950-
dc.description.abstractWe have previously demonstrated that enzymatic digestion of chondroitin sulfate proteoglycan (CSPG) at the scar promotes the axonal regrowth of Clarke's nucleus (CN) neurons into an implanted peripheral nerve graft after hemisection of the spinal cord. The present study examined whether degradation of CSPG using chondroitinase ABC promoted the regeneration of CN neurons through the scar into the rostral spinal cord in neonatal and adult rats. Following hemisection of the spinal cord at T11, either vehicle or chondroitinase ABC was applied onto the lesion site. The postoperative survival periods were 2 and 4 weeks. The regenerated CN neurons were retrogradely labeled by Fluoro-Gold injected at spinal cord level C7. In the sham group, there was no regeneration of injured CN neurons in both neonatal and adult rats. Treatment with 2.5 unit/ml chondroitinase ABC in neonates resulted in 11.8 and 8.3% of the injured CN neurons regenerated into the rostral spinal cord at 2 and 4 weeks, respectively. In adults, 9.4 and 12.3%, at 2 and 4 weeks, respectively, of the injured CN neurons regenerated their axons to the rostral spinal cord. The immunoreactivity for the carbohydrate epitope of CSPG was dramatically decreased around the lesion site after treatment with chondroitinase ABC compared to sham control in both neonatal and adult animals. Our results show that axonal regeneration in the spinal cord can be promoted by degradation of CSPG with chondroitinase ABC. This result further suggests that CSPG is inhibitory to the regeneration of neurons in the spinal cord after traumatic injury. © 2003 Elsevier Science (USA). All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexnren_HK
dc.relation.ispartofExperimental Neurologyen_HK
dc.subjectAxotomyen_HK
dc.subjectChondroitin sulfateen_HK
dc.subjectProteoglycansen_HK
dc.subjectRegrowthen_HK
dc.subjectSpinal corden_HK
dc.subjectTraumatic injuryen_HK
dc.subject.meshAge Factorsen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAnimals, Newbornen_HK
dc.subject.meshAxons - drug effects - physiologyen_HK
dc.subject.meshChondroitin ABC Lyase - pharmacologyen_HK
dc.subject.meshChondroitin Sulfate Proteoglycans - drug effects - metabolismen_HK
dc.subject.meshChondroitin Sulfates - biosynthesisen_HK
dc.subject.meshCicatrix - pathologyen_HK
dc.subject.meshDisease Models, Animalen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshNerve Regeneration - drug effectsen_HK
dc.subject.meshNeurons - drug effects - pathology - physiologyen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshSpinal Cord Injuries - drug therapy - pathologyen_HK
dc.titleAxonal regeneration of Clarke's neurons beyond the spinal cord injury scar after treatment with chondroitinase ABCen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0014-4886&volume=182&spage=160&epage=168&date=2002&atitle=Axonal+regeneration+of+Clarke%27s+neurons+beyond+the+spinal+cord+injury+scar+after+treatment+with+chondroitinase+ABCen_HK
dc.identifier.emailCheung, PT:ptcheung@hkucc.hku.hken_HK
dc.identifier.emailSo, KF:hrmaskf@hkucc.hku.hken_HK
dc.identifier.emailWu, W:wtwu@hkucc.hku.hken_HK
dc.identifier.authorityCheung, PT=rp00351en_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.identifier.authorityWu, W=rp00419en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0014-4886(02)00052-3en_HK
dc.identifier.pmid12821386-
dc.identifier.scopuseid_2-s2.0-0037757588en_HK
dc.identifier.hkuros76873en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037757588&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume182en_HK
dc.identifier.issue1en_HK
dc.identifier.spage160en_HK
dc.identifier.epage168en_HK
dc.identifier.isiWOS:000183837400015-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYick, LW=6603414804en_HK
dc.identifier.scopusauthoridCheung, PT=7202595465en_HK
dc.identifier.scopusauthoridSo, KF=34668391300en_HK
dc.identifier.scopusauthoridWu, W=7407081122en_HK

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