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I. Iandiev, T. Pannicke, A. Wurm, S. Uhlmann, A. Reichenbach, P. Wiedemann, A. Bringmann; Müller Glial Cells Response to Light-Induced Retinal Degeneration. Invest. Ophthalmol. Vis. Sci. 2007;48(13):2506.
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Apoptosis of photoreceptors occurs in retinal dystrophies, e.g., during retinitis pigmentosa or age-related macula degeneration. It is also observed after light-induced degeneration, which is studied in animal models. Whereas the behaviour of photoreceptors after light damage is well documented, much less is known about the involvement of retinal Müller glial cells.
We investigated Müller cells after light-evoked degeneration by immunocytochemistry, microfluorimetry, and patch-clamp recording. One eye of pigmented rats was exposed to blue light for 30 min.
After 3 days, immunostaining of the retinal tissue revealed an upregulation of glial fibrillary acidic protein, a marker of gliosis in Müller cells, mainly at the edge of the exposed area. Moreover, the expression of aquaporin-4 was increased in the outer nuclear layer of the degenerating region. The immunostaining for the inwardly rectifying K+ channel, Kir4.1, was decreased and showed a uniform distribution, whereas this protein is concentrated around blood vessels and at the inner limiting membrane in control retinae. Alterations in Kir4.1 staining corresponded well with a decrease of the inward currents in isolated Müller cells (to about 20%, Fig. 1) accompanied by lower membrane potentials. Most of the Müller cells from the light-exposed area displayed fast transient (A-type) outward K+ currents, which are not recorded in control cells. Moreover, we studied the behaviour of Müller cells in retinal slices under hypoosmotic stress. Müller cells were selectively stained with the fluorescent dye, Mitotracker Orange. Application of a hypotonic solution had no effect on Müller cells from control tissue, whereas Müller cells in slices from light-damaged retinae displayed a swelling of their somata.
We assume that altered expression of K+ and water channels might be a response of Müller cells to osmotic imbalances in the outer retina after light-induced photoreceptor apoptosis.
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