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M. Nishimura, T. Kurimoto, Y. Tagami, S. Oono, O. Mimura; 2-Adrenergic Agonists Enhance Retinal Ganglion Cell Axonal Regeneration via CNTF Production in Muller Cells. Invest. Ophthalmol. Vis. Sci. 2007;48(13):2453.
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© ARVO (1962-2015); The Authors (2016-present)
α2-Adrenergic agonists (A2 agonists), such as xylazine, are used as sedatives and analgesics for various animals. In adult rats, these agonists promote axonal regeneration after optic nerve crush injury and also protect against photoreceptor damage via upregulation of fibroblast growth factor-2. However, the mechanism by which A2 agonists promote axonal regeneration is not fully clear. We investigated whether A2 agonists promote endogenous neurotrophic factor production in the rat retina by assessing the expression of FGF, BDNF, CNTF, and trkB mRNAs.
In adult Wistar rats, the optic nerve was crushed by microforceps, and A2 agonists (xylazine or clonidine) were injected as a single dose or daily. On days 1, 3, and 7, total RNA was extracted from the retina and RT-PCR was used to determine the expression of neurotrophic factor mRNAs. To examine the retinal expression of neurotrophic factors, imunohistochemistry was also performed.
A2 agonists enhanced CNTF mRNA expression, and daily treatment was more effective than a single dose. An A2 antagonist markedly inhibited CNTF induction. CNTF was imunohistochemically localized in Muller cells.
Promotion of axonal regeneration by A2 agonists involves the upregulation of endogenous CNTF production in Muller cells.
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