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V. Canto Soler, V. Torbidoni, M.J. Villar, A.M. Suburo; Purinergic Receptors in Astrocytes of the Retina . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4564.
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Purpose: ATP receptors of the P2Y family have been involved in astrogliosis. Besides, P2Y2 mRNA is present in Müller cells and increases in viral retinopathy. To test whether this receptor is also involved in light-induced retinal gliosis, we made an immunohistochemical study of P2Y2 in mice retinas submitted to different periods of continuous illumination. Methods: Male BALB-c mice were exposed to 1,500 lux illumination for 3, 6, 9 and 18 days. Animals were euthanized and fixed for immunohistochemistry using antibodies against P2Y2, glial fibrillary acidic protein (GFAP) and endothelin, a selective marker of retinal astrocytes. Consecutive sections were stained with neutral red. Results: In normal retinas, P2Y2 exclusively labeled a monolayer of stellate cells lying beneath the vitreal surface. There was perfect co-localization between P2Y2, GFAP and endothelin immunoreactivities, indicating that P2Y2 was expressed in astrocytes. Under continuous illumination, reduction of the outer nuclear layer (ONL) was detected after day 6. By day 18, the ONL had disappeared almost completely. GFAP immunoreactivity, however, was already increased after day 3, both in astrocytes and Müller cells. P2Y2 staining was also increased, but remained restricted to astrocytes, as demonstrated by identical behavior of endothelin immunoreactivity. Both markers showed an increase in the number of astrocyte cell bodies and processes. At the end of the experimental period, some labeled processes extended within the inner plexiform and nuclear layers. Conclusions: The ATP receptor P2Y2 is expressed by retinal astrocytes but not by Müller cells. Light-induced retinal degeneration is accompanied by an early increase in the number of astrocyte cell bodies and processes expressing this receptor. These observations support a possible role of extracellular nucleotides in the induction of reactive gliosis.
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