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Invest Ophthalmol Vis Sci. 2008 Aug;49(8):3559-67. doi: 10.1167/iovs.08-1723. Epub 2008 Apr 30.

Müller cell response to blue light injury of the rat retina.

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1
Department of Ophthalmology and Eye Clinic, Translational Center for Regenerative Medicine, Faculty of Medicine, University of Leipzig, Leipzig, Germany.

Abstract

PURPOSE:

In addition to photoreceptor degeneration, excessive light causes degenerative alterations in the inner retina and ganglion cell death. A disturbance in osmohomeostasis may be one causative factor for the alterations in the inner retina. Because Müller cells mediate inner retinal osmohomeostasis (mainly through channel-mediated transport of potassium ions and water), the authors investigated whether these cells alter their properties in response to excessive blue light.

METHODS:

Retinas of adult rats were exposed to blue light for 30 minutes. At various time periods after treatment, retinal slices were immunostained against glial fibrillary acidic protein and potassium and water channel proteins (Kir4.1, aquaporin-1, aquaporin-4). Patch-clamp recordings of potassium currents were made in isolated Müller cells, and the swelling of Müller cell bodies was recorded in retinal slices.

RESULTS:

After blue light treatment, Müller cells displayed hypertrophy and increased glial fibrillary acidic protein. The immunostaining of the glial water channel aquaporin-4 was increased in the outer retina, whereas the immunostaining of the photoreceptor water channel aquaporin-1 disappeared. Blue light treatment resulted in a decrease and a dislocation of the Kir4.1 protein in the whole retinal tissue and a decrease in the potassium conductance of Müller cells. Hypo-osmotic stress evoked a swelling of Müller cell bodies in light-treated retinas that was not observed in control tissues.

CONCLUSIONS:

The decrease in functional Kir channels may result in a disturbance of retinal potassium and water homeostasis, contributing to the degenerative alterations of the inner retina after exposure to blue light.

PMID:
18450590
DOI:
10.1167/iovs.08-1723
[Indexed for MEDLINE]
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