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P<P, published online ahead of print April 30, 2008
(Investigative Ophthalmology and Visual Science. )
© 2008 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.08-1723

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Article

Muller Cell Response to Blue Light Injury of the Rat Retina

Ianors Iandiev 1, Antje Wurm 2, Margrit Hollborn 1, Peter P. Wiedemann 3, Christian Grimm 4, Charlotte E. Reme 4, Andreas Reichenbach 2, Thomas Pannicke 2, and Andreas Bringmann 5*

1 Dep. of Ophthalmology, Eye Clinic, University of Leipzig, Leipzig, Germany
2 Paul Flechsig Institute of Brain Research, University of Leipzig, Leipzig, Germany
3 Universitaet Leipzig, Eye Hospital, Leipzig, Germany
4 Laboratory for Retinal Cell Biology, University Eye Hospital, Zurich, Zurich, Switzerland
5 Department of Ophthalmology, Eye Clinic, University of Leipzig, Liebigstrasse 10-14, Leipzig, D-04103, Germany

* To whom correspondence should be addressed. E-mail: bria{at}medizin.uni-leipzig.de.


   Abstract

PURPOSE. In addition to photoreceptor degeneration, excessive light causes degenerative alterations in the inner retina and ganglion cell death. A disturbance in the osmohomeostasis may be one causative factor for the alterations in the inner retina. Since Muller cells mediate the inner retinal osmohomeostasis (mainly via channel-mediated transport of potassum ions and water), we 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, aquaporins-1 and -4). Patch-clamp recordings of potassium currents were made in isolated Muller cells, and the swelling of Muller cell bodies was recorded in retinal slices. RESULTS. After blue light treatment, Muller cells displayed hypertrophy and an increase in glial fibrillary acidic protein. The immunostaining of the glial water channel aquaporin-4 was increased in the outer retina while the immunostaining of the photoreceptor water channel aquaporin-1 disappeared. Blue light treatment resulted in a decrease and mislocation of the Kir4.1 protein in the whole retinal tissue, and a decrease in the potassium conductance of Muller cells. Hypoosmotic stress evoked a swelling of Muller 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 the retinal potassium and water homeostasis contributing to the degenerative alterations of the inner retina after exposure to blue light.

Key Words: light damage, Mueller cell, potassium transport







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