Abstract

FR.14.05

Glial cell response in the light-damaged retina

Yandiev Y., Bringmann A.
Translational Center for Regenerative Medicine and Department of Ophthalmology and Eye Clinic, University of Leipzig, Leipzig

Objective: Excessive light exposure causes photoreceptor degeneration and is associated with oxidative stress and inflammation. We investigated whether exposure of the rat retina to blue light causes gliotic alterations of Müller cells which are known to occur during retinal ischemia-reperfusion or ocular inflammation.
Methods: One eye of pigmented rats was exposed to blue light (405 nm) for 30 min. Three days after, immunohistochemistry, single-cell electrophysiology, and cell swelling experiments were carried out.
Results: Exposure to blue light caused an upregulation of glial fibrillary acidic protein, a marker of gliosis in Müller cells, especially in the transition zone between the injured and uninjured retinal areas. The expression of the glial water channel, aquaporin-4, was increased in the outer nuclear layer in the injured region. The immunostaining for the glial potassium channel, Kir4.1, was decreased and showed a uniform distribution in the injured retina, whereas this protein was concentrated around blood vessels and at the limiting membranes in control retinas. The alterations in retinal Kir4.1 staining corresponded with a decrease in the potassium conductance of isolated Müller cells (to ~20%). The osmotic volume regulation of Müller cells alters after light exposure. Application of a hypotonic solution had no effect on the size of Müller cell bodies in control tissues, whereas Müller cells in slices from light-damaged retinas displayed a swelling of their somata.
Conclusions: Since similar gliotic responses (decrease in potassium conductance and induction of osmotic cell swelling) were previously observed during retinal ischemia-reperfusion and ocular inflammation, we assume that oxidative stress and retinal inflammation are causative factors of Müller cell gliosis after exposure to blue light. Alterations in the expression of glial potassium and water channels may represent a response to the ionic and osmotic imbalances in the outer retina caused by photoreceptor apoptosis, and may contribute to retinal degeneration.

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