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Altered membrane physiology in Müller glial cells after transient ischemia of the rat retina

✍ Scribed by Thomas Pannicke; Ortrud Uckermann; Ianors Iandiev; Bernd Biedermann; Peter Wiedemann; Ido Perlman; Andreas Reichenbach; Andreas Bringmann

Publisher
John Wiley and Sons
Year
2004
Tongue
English
Weight
285 KB
Volume
50
Category
Article
ISSN
0894-1491

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✦ Synopsis

Inwardly rectifying K+ (Kir) channels have been implicated in the mediation of retinal K+ homeostasis by Muller glial cells. To assess possible involvement of altered glial K+ channel expression in ischemia-reperfusion injury, transient retinal ischemia was induced in rat eyes. Acutely isolated Muller cells from postischemic retinae displayed a fast downregulation of their Kir currents, which began within 1 day and reached a maximum at 3 days of reperfusion, with a peak decrease to 20% as compared with control. This strong decrease of Kir currents was accompanied by an increase of the incidence of cells which displayed depolarization-evoked fast transient (A-type) K+ currents. While no cell from untreated control rats expressed A-type K+ currents, all cells investigated from 3- and 7-day postischemic retinae displayed such currents. An increased incidence of cells displaying fast transient Na+ currents was observed at 7 days after ischemia. These results suggest a role of altered glial Kir channel expression in postischemic neuronal degeneration via disturbance of retinal K+ siphoning.

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