Nogo receptor deletion and multimodal exercise improve distinct aspects of recovery in cervical spinal cord injury

Noam Y. Harel, Kang Ho Song, Xin Tang, Stephen M. Strittmatter

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


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.

Original languageEnglish
Pages (from-to)2055-2066
Number of pages12
JournalJournal of Neurotrauma
Issue number11
StatePublished - 1 Nov 2010
Externally publishedYes


  • Nogo
  • Nogo receptor
  • incomplete spinal cord injury
  • plasticity
  • rehabilitation
  • task specificity


Dive into the research topics of 'Nogo receptor deletion and multimodal exercise improve distinct aspects of recovery in cervical spinal cord injury'. Together they form a unique fingerprint.

Cite this