Effect of the adenosine A1 receptor agonist on demyelination and remyelination processes in lysolecithin induced demyelination in rat optic chiasm

Asghari, A.A. and Azarnia, M. and Mirnajafi-Zadeh, S.J. and Javan, M. (2012) Effect of the adenosine A1 receptor agonist on demyelination and remyelination processes in lysolecithin induced demyelination in rat optic chiasm. Feyz Journal of Kashan University of Medical Sciences, 16.

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Official URL: http://feyz.kaums.ac.ir/article-1-1366-en.html
DOI: UNSPECIFIED

Abstract

Background: Demyelination in central nervous system is usually followed by remyelination however, chronic lesions with subsequent functional impairment result from the eventual failure of remyelination process, as seen in multiple sclerosis. Remyelination is the process through which oligodendrocyte-progenitor cells (OPCs) restore new myelin sheathes around demyelinated axons. This study aimed to investigate the effect of A1 receptor agonist, N6-cyclohexyladenosine (CHA), on the demyelination and remyelination processes in rat optic chiasm following lysophosphatidylcholine (LPC)-induced demylination. Materials and Methods: In this experimental study, LPC was injected into the optic chiasm of three groups of rats (n=6). Control group received aCSF on different days following LPC injection. Two groups of animals received CHA on days 0-14 or 14-28 post-lesion. Demyelination and remyelination levels were evaluated by recording visual evoked potential (VEP) from the scalp.Results: The highest level of demyelination was occurred on day 7 post-lesion LPC injection and gradually reduced during the days 7-28. The P-wave latency was significantly increased on day 7 and then partially restored during the days 7-28 post-lesion. CHA administration during the days 0-14 attenuated demyelination process. In addition, CHA administration in remyelination phase (days 14-28) was able to potentiate the endogenous myelin repair.Conclusion: Injection of CHA could prevent the lysolecithin-induced variations in VEP. The effects of CHA may be mediated through increment of OPCs proliferation and their differentiation into myelinating oligodendrocytes.

Item Type: Article
Subjects: Neuroscience
Divisions: Feyz journal
Depositing User: ART . editor
Date Deposited: 09 May 2017 14:42
Last Modified: 23 May 2017 13:40
URI: http://eprints.kaums.ac.ir/id/eprint/1883

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