| Nogo receptor deletion and multimodal exercise improve distinct aspects of recovery in cervical spinal cord injury. | |
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MedLine Citation:
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PMID: 20809785 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We tested the ability of two plasticity-promoting approaches to enhance recovery in a mouse model of incomplete spinal cord injury (SCI). Genetically, we reduced myelin-mediated inhibition of neural plasticity through Nogo66-receptor (NgR) gene deletion. Behaviorally, we utilized a novel multimodal exercise training paradigm. Adult mice of wild-type or NgR-null genotype were subjected to partial lateral hemisection (LHx) at C3-C4 with the intent of producing anatomically and functionally mild deficits. Exercise training or control treatment proceeded for 14 weeks. Behavioral outcomes were assessed prior to tract tracing and histological analysis. Genotype and training exerted differing effects on performance; training improved performance on a test related to the training regimen (task-specific benefit), whereas genotype also improved performance on more generalized behaviors (task-non-specific benefit). There were no significant histological differences across genotype or training assignment with regard to lesion size or axonal tract staining. Thus either NgR gene deletion or exercise training benefits mice with mild cervical spinal injury. In this lesion model, the effects of NgR deletion and training were not synergistic for the tasks assessed. Further work is required to optimize the interaction between pharmacological and physical interventions for SCI. |
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Authors:
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Noam Y Harel; Kang-Ho Song; Xin Tang; Stephen M Strittmatter |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of neurotrauma Volume: 27 ISSN: 1557-9042 ISO Abbreviation: J. Neurotrauma Publication Date: 2010 Nov |
Date Detail:
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Created Date: 2010-11-22 Completed Date: 2011-03-03 Revised Date: 2011-12-16 |
Medline Journal Info:
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Nlm Unique ID: 8811626 Medline TA: J Neurotrauma Country: United States |
Other Details:
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Languages: eng Pagination: 2055-66 Citation Subset: IM |
Affiliation:
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Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, Connecticut 06520-8018, USA. noam.harel@yale.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Behavior, Animal / physiology Exercise Therapy* Female GPI-Linked Proteins / genetics, physiology Gene Deletion Genotype Hand Strength / physiology Immunohistochemistry Male Mice Mice, Inbred C57BL Myelin Proteins / genetics*, physiology Neuronal Plasticity / physiology Physical Conditioning, Animal Postural Balance / physiology Receptors, Cell Surface / genetics*, physiology Reproducibility of Results Serotonin / metabolism Spinal Cord / pathology Spinal Cord Injuries / pathology, rehabilitation*, therapy* Walking / physiology |
| Grant Support | |
ID/Acronym/Agency:
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R01 NS039962-11/NS/NINDS NIH HHS; R01 NS042304-09/NS/NINDS NIH HHS; R37 NS033020-19/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/GPI-Linked Proteins; 0/Myelin Proteins; 0/Receptors, Cell Surface; 0/Rtn4r protein, mouse; 50-67-9/Serotonin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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