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Conference Paper: Lithium chloride and chondroitinase ABC promote axonal regeneration of rubrospinal neurons after spinal cord injury

TitleLithium chloride and chondroitinase ABC promote axonal regeneration of rubrospinal neurons after spinal cord injury
Authors
Issue Date2004
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neulet
Citation
The 23rd Scientific Meeting of the Hong Kong Society of Neurosciences. Hong Kong, 2004. In Neuroscience Letters, 2004, v. 370 suppl., p. S38-S39 How to Cite?
AbstractAxons in the spinal cord fail to regenerate spontaneously after injury. We examined whether chondroitinase ABC (ChABC) promote the axonal regeneration of rubrospinal tract (RST) neurons following injury of the spinal cord. We also assessed the effect of lithium chloride (LiCl) on the regeneration of RST neurons in the injured spinal cord. Adult female Sprague–Dawley rats were used in this study. Under anesthesia with ketamine and xylazine, the animals received a unilateral hemisection at the seventh cervical spinal cord segment (C7). Four weeks after the injury, regeneration of RST axons across the lesion scar was examined by injection of Fluoro-Gold at spinal segment T2. The recovery of motor function was studied on a test of forelimb usage. RST neurons did not regenerate their axons after spinal cord injury. Intraperitoneal injection of LiCl alone did not promote the axonal regeneration of RST neurons. Administration of ChABC at the lesion site promoted the regeneration of RST axons by 20%. Combined treatment of LiCl together with ChABC significantly increased the regeneration of RST axons to 42%. Animals receiving the combined treatment used both forelimbs together more often than animals received sham or single treatment. Immunoblotting and immunohistochemical analysis revealed that administration of LiCl induced the expression of inactive GSK-3 and the upregulation of Bcl-2 in RST neurons after spinal cord injury. These results suggest that LiCl inhibits GSK-3 and reinforces the regeneration-promoting effect of ChABC through a Bcl-2 dependent mechanism. Combined use of LiCl together with ChABC could be a potential treatment for spinal cord injury. Acknowledgment: This study was supported by the University of Hong Kong.
Persistent Identifierhttp://hdl.handle.net/10722/95387
ISSN
2015 Impact Factor: 2.107
2015 SCImago Journal Rankings: 1.035

 

DC FieldValueLanguage
dc.contributor.authorYick, LWen_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorWu, Wen_HK
dc.date.accessioned2010-09-25T16:00:41Z-
dc.date.available2010-09-25T16:00:41Z-
dc.date.issued2004en_HK
dc.identifier.citationThe 23rd Scientific Meeting of the Hong Kong Society of Neurosciences. Hong Kong, 2004. In Neuroscience Letters, 2004, v. 370 suppl., p. S38-S39en_HK
dc.identifier.issn0304-3940en_HK
dc.identifier.urihttp://hdl.handle.net/10722/95387-
dc.description.abstractAxons in the spinal cord fail to regenerate spontaneously after injury. We examined whether chondroitinase ABC (ChABC) promote the axonal regeneration of rubrospinal tract (RST) neurons following injury of the spinal cord. We also assessed the effect of lithium chloride (LiCl) on the regeneration of RST neurons in the injured spinal cord. Adult female Sprague–Dawley rats were used in this study. Under anesthesia with ketamine and xylazine, the animals received a unilateral hemisection at the seventh cervical spinal cord segment (C7). Four weeks after the injury, regeneration of RST axons across the lesion scar was examined by injection of Fluoro-Gold at spinal segment T2. The recovery of motor function was studied on a test of forelimb usage. RST neurons did not regenerate their axons after spinal cord injury. Intraperitoneal injection of LiCl alone did not promote the axonal regeneration of RST neurons. Administration of ChABC at the lesion site promoted the regeneration of RST axons by 20%. Combined treatment of LiCl together with ChABC significantly increased the regeneration of RST axons to 42%. Animals receiving the combined treatment used both forelimbs together more often than animals received sham or single treatment. Immunoblotting and immunohistochemical analysis revealed that administration of LiCl induced the expression of inactive GSK-3 and the upregulation of Bcl-2 in RST neurons after spinal cord injury. These results suggest that LiCl inhibits GSK-3 and reinforces the regeneration-promoting effect of ChABC through a Bcl-2 dependent mechanism. Combined use of LiCl together with ChABC could be a potential treatment for spinal cord injury. Acknowledgment: This study was supported by the University of Hong Kong.-
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neuleten_HK
dc.relation.ispartofNeuroscience Lettersen_HK
dc.rightsNeuroscience Letters. Copyright © Elsevier Ireland Ltd.en_HK
dc.titleLithium chloride and chondroitinase ABC promote axonal regeneration of rubrospinal neurons after spinal cord injuryen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0304-3940&volume=370 supplement&spage=S38&epage=&date=2004&atitle=Lithium+chloride+and+chondroitinase+ABC+promote+axonal+regeneration+of+rubrospinal+neurons+afte+spinal+cord+injuryen_HK
dc.identifier.emailYick, LW: yickkevinhk@yahoo.comen_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.identifier.doi10.1016/j.neulet.2004.09.001-
dc.identifier.hkuros108000en_HK
dc.identifier.volume370en_HK
dc.identifier.issuesuppl.-
dc.identifier.spageS38en_HK
dc.identifier.epageS39-

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