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

Abstract:

: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.

journal_name

Glia

journal_title

Glia

authors

Pannicke T,Uckermann O,Iandiev I,Biedermann B,Wiedemann P,Perlman I,Reichenbach A,Bringmann A

doi

10.1002/glia.20151

subject

Has Abstract

pub_date

2005-04-01 00:00:00

pages

1-11

issue

1

eissn

0894-1491

issn

1098-1136

journal_volume

50

pub_type

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