Systemic administration of valproic acid stimulates overexpression of microtubule-associated protein 2 in the spinal cord injury model to promote neurite outgrowth
Growing body of evidence suggests that neurite outgrowth is a key determinant in the re-networking of damaged neuronal circuits as well as synaptogenesis. The essential molecule in this interesting process is microtubule-associated protein 2 (MAP2) studies demonstrated that inhibition of MAP2 by ant...
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Published in | Neurological research (New York) Vol. 37; no. 3; p. 223 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
England
01.03.2015
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Subjects | |
Online Access | Get more information |
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Summary: | Growing body of evidence suggests that neurite outgrowth is a key determinant in the re-networking of damaged neuronal circuits as well as synaptogenesis. The essential molecule in this interesting process is microtubule-associated protein 2 (MAP2) studies demonstrated that inhibition of MAP2 by antisense Oligonucleotide hinders neurite outgrowth.
In the current study, we evaluated the effects of valproic acid (VPA), a histone deacetylase inhibitor on the expression of MAP2 in the rat spinal cord injury model by real time RT-PCR and immunoreactivity assays.
We revealed that a significant increase in the MAP2 overexpression occurred in VPA-treated group compared to the sham group by quantitative real-time reverse transcription polymerase chain reaction (RT-PCR) and immunoreactivity assays for MAP2 gene expression.
The present findings indicated that systemic administration of VPA stimulated MAP2 gene expression and also supports the involvement of the MAP2-mediated de novo re-arborization and neurite outgrowth of neurons, which might contribute to successful neuronal re-wirings. Thus, VPA has promising applications in the treatment of many neurological problems, such as neurotrauma, Alzheimer and Parkinson's disease, and others. |
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ISSN: | 1743-1328 |
DOI: | 10.1179/1743132814Y.0000000438 |