Document Detail

Upregulation and colocalization of p75 and Nav1.8 in Purkinje neurons in experimental autoimmune encephalomyelitis.
MedLine Citation:
PMID:  15464262     Owner:  NLM     Status:  MEDLINE    
Recent studies have indicated that, in addition to demyelination and axonal degeneration, a third factor, dysregulated ion channel expression, contributes to the pathophysiology of experimental autoimmune encephalomyelitis (EAE) and multiple sclerosis (MS). Consistent with this suggestion, upregulated expression of sodium channel Na(v)1.8 is observed in Purkinje neurons in EAE and MS, and biophysical studies indicate that aberrant expression of Na(v)1.8 produces abnormal Purkinje cell firing which may contribute to the development of cerebellar ataxia. However, the molecular mechanisms that contribute to the upregulation of Na(v)1.8 in Purkinje cells in EAE and MS have not yet been determined. Previous studies have shown that neurotrophic factors can modulate sodium channel expression and that elevated levels of NGF are present in EAE and MS. Using immunocytochemical methods, we examined the relationship between the upregulation of Na(v)1.8 and the expression of the NGF receptors p75 and TrkA in EAE. Here we demonstrate that upregulation of Na(v)1.8 is associated with expression of p75 and low levels of TrkA in the majority of Purkinje cells in EAE. These findings, together with previous studies demonstrating a modulatory role of NGF on sodium channel expression, suggest that NGF acting via p75 contributes to the upregulation of Na(v)1.8 in Purkinje cells in EAE.
Tina G Damarjian; Matthew J Craner; Joel A Black; Stephen G Waxman
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Neuroscience letters     Volume:  369     ISSN:  0304-3940     ISO Abbreviation:  Neurosci. Lett.     Publication Date:  2004 Oct 
Date Detail:
Created Date:  2004-10-06     Completed Date:  2005-01-13     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  7600130     Medline TA:  Neurosci Lett     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  186-90     Citation Subset:  IM    
Department of Neurology, The Center for Neuroscience and Regeneration Research, Yale University School of Medicine, LCI 707, 333 Cedar Street, P.O. Box 208018, New Haven, CT 06520-8018, USA.
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MeSH Terms
Adaptor Proteins, Signal Transducing
Disease Models, Animal
Encephalomyelitis, Autoimmune, Experimental / chemically induced,  metabolism*
Fluorescent Antibody Technique / methods
Glycoproteins / metabolism
Peptide Fragments / metabolism
Purkinje Cells / metabolism*
Receptor, trkA / metabolism
Sodium Channels / metabolism*
Trans-Activators / metabolism*
Transcription Factors
Reg. No./Substance:
0/Adaptor Proteins, Signal Transducing; 0/Glycoproteins; 0/Peptide Fragments; 0/Psip1 protein, mouse; 0/Sodium Channels; 0/Trans-Activators; 0/Transcription Factors; 0/myelin oligodendrocyte glycoprotein (35-55); 0/sensory neuron specific (SNS) sodium channel; EC, trkA

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