Müller cell response to blue light injury of the rat retina.
OBJECTIVE
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.
Iandiev
Ianors
I
Department of Ophthalmology and Eye Clinic, Translational Center for Regenerative Medicine, Faculty of Medicine, University of Leipzig, Leipzig, Germany.
Wurm
Antje
A
Hollborn
Margrit
M
Wiedemann
Peter
P
Grimm
Christian
C
Remé
Charlotte E
CE
Reichenbach
Andreas
A
Pannicke
Thomas
T
Bringmann
Andreas
A
D000818:Animals; D051398:Aquaporin 1 / Q000378:metabolism; D051401:Aquaporin 4 / Q000378:metabolism; D001834:Body Water / Q000378:metabolism; D016923:Cell Death; D019084:Fluorescent Antibody Technique, Indirect; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D008027:Light; D009457:Neuroglia / Q000502:physiology*; D018408:Patch-Clamp Techniques; D020419:Photoreceptor Cells, Vertebrate / Q000473:pathology; D010857:Pigment Epithelium of Eye / Q000473:pathology; D011188:Potassium / Q000378:metabolism; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism; D011833:Radiation Injuries, Experimental / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D020318:Rats, Long-Evans; D012160:Retina / Q000473:pathology / Q000528:radiation effects*; D012162:Retinal Degeneration / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D015854:Up-Regulation; D000098854:Kcnj10 Channel
C496022:Aqp1 protein, rat; C496032:Aqp4 protein, rat; D051401:Aquaporin 4; D005904:Glial Fibrillary Acidic Protein; D000098854:Kcnj10 Channel; D024661:Potassium Channels, Inwardly Rectifying; D051398:Aquaporin 1; D011188:Potassium