Document Detail


NCAM-mediated locomotor recovery from spinal cord contusion injury involves neuroprotection, axon regeneration, and synaptogenesis.
MedLine Citation:
PMID:  20381564     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The expression level of neural cell adhesion molecule (NCAM), which plays a critical role in pathways involving development and plasticity of the nervous system, changes markedly after spinal cord injury (SCI). However, the significance of NCAM-involved mechanisms in SCI remains elusive. The present study demonstrates that NCAM-deficient (ND) mice exhibited significantly poorer locomotor activity than wildtype (WT) littermates with the same injury intensity by the contusion model. To determine detailed contribution of NCAM, quantitative immunohistochemistry examination was performed on the injured spinal cord of 6mm along the rostrocaudal axis in the animals for up to 5 weeks after SCI. Overall level of NCAM decreased initially in the lesion site but increased around the center of the injury thereafter. At acute stage, more apoptotic cells were found in the gray and white matter in ND mice. Between the two animal groups, no obvious difference in expression levels of GFAP (astrocytosis marker) and MBP (remyelination marker) was detected. However, diverse expression trends of NF200 (axon marker), GAP-43 (synaptogenesis indicator) and phosphorylated ERK (active signal molecule) were observed in the area encompassing the lesion site, and remarkable differences were illustrated between WT mice and ND littermates. Detailed analysis indicates that NCAM-mediated pathways may be involved in the activation of ERK at acute stages and bi-phasic upregulation of GAP-43 expression at acute and sub-acute stages after SCI to promote cell survival, outgrowth of regenerated axons, synaptogenesis, and function recovery.
Authors:
Si Zhang; Yin Yan Xia; Han Chi Lim; Feng Ru Tang; Zhi Wei Feng
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-04-08
Journal Detail:
Title:  Neurochemistry international     Volume:  56     ISSN:  1872-9754     ISO Abbreviation:  Neurochem. Int.     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-05-18     Completed Date:  2010-11-29     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8006959     Medline TA:  Neurochem Int     Country:  England    
Other Details:
Languages:  eng     Pagination:  919-29     Citation Subset:  IM    
Copyright Information:
2010 Elsevier Ltd. All rights reserved.
Affiliation:
School of Biological Science, Nanyang Technological University, 60 Nanyang Drive, Singapore 637551, Singapore.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / physiology
Cell Survival / physiology
Disease Models, Animal
Enzyme Activation / physiology
Extracellular Signal-Regulated MAP Kinases / physiology
Female
Gliosis / pathology
Growth Cones / pathology*,  physiology,  ultrastructure
Hindlimb / innervation
Mice
Mice, Inbred C57BL
Mice, Transgenic
Motor Activity / physiology*
Nerve Regeneration / physiology*
Neural Cell Adhesion Molecules / genetics,  physiology*
Neural Pathways / physiology
Neuronal Plasticity / physiology*
Recovery of Function / physiology*
Spinal Cord Injuries / metabolism*,  pathology,  therapy*
Synapses / physiology
Chemical
Reg. No./Substance:
0/Neural Cell Adhesion Molecules; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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