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
Gliajournal_title
Gliaauthors
Pannicke T,Uckermann O,Iandiev I,Biedermann B,Wiedemann P,Perlman I,Reichenbach A,Bringmann Adoi
10.1002/glia.20151subject
Has Abstractpub_date
2005-04-01 00:00:00pages
1-11issue
1eissn
0894-1491issn
1098-1136journal_volume
50pub_type
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