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GAP‐43 gene expression is increased in anterior horn cells of amyotrophic lateral sclerosis
Author(s) -
Parhad Irma M.,
Oishi Roderick,
Clark Arthur W.
Publication year - 1992
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410310605
Subject(s) - amyotrophic lateral sclerosis , synaptogenesis , in situ hybridization , motor neuron , biology , anterior horn cell , messenger rna , neuroscience , gap 43 protein , anatomy , microbiology and biotechnology , pathology , spinal cord , gene , medicine , immunohistochemistry , immunology , disease , biochemistry
In amyotrophic lateral sclerosis (ALS), neuronal loss and axonal degeneration occur in motor neurons. Although there is limited axonal regeneration, surviving motor neurons send collateral sprouts to denervated muscle fibers. GAP‐43, a protein enriched in growth cones and synaptic terminals, is thought to have a role in axonal elongation and synaptogenesis. GAP‐43 messenger RNA (mRNA) expression was evaluated in ALS spinal cords using Northern blot analysis and in situ hybridization to assess whether surviving neurons can mount an appropriate response to injury. There was a two‐ to four‐fold increase in GAP‐43 mRNA in ALS that localized to the anterior horn cells. The increase in GAP‐43 mRNA indicates that the mechanism which leads to degeneration in ALS does not compromise the neuron's capacity for vigorous expression of growth‐associated proteins.