Systemic administration of valproic acid stimulates overexpression of microtubule-associated protein 2 in the spinal cord injury model to promote neurite outgrowth.

OBJECTIVES

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.

METHODS

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.

RESULTS

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.

DISCUSSION: 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.