TY - JOUR
T1 - Altered membrane physiology in Müller glial cells after transient ischemia of the rat retina
AU - Pannicke, Thomas
AU - Uckermann, Ortrud
AU - Iandiev, Ianors
AU - Biedermann, Bernd
AU - Wiedemann, Peter
AU - Perlman, Ido
AU - Reichenbach, Andreas
AU - Bringmann, Andreas
PY - 2005/4/1
Y1 - 2005/4/1
N2 - Inwardly rectifying K+ (Kir) channels have been implicated in the mediation of retinal K+ homeostasis by Müller 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 Müller 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.
AB - Inwardly rectifying K+ (Kir) channels have been implicated in the mediation of retinal K+ homeostasis by Müller 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 Müller 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.
KW - Glia
KW - Inwardly rectifying potassium channel
KW - Ischemia-reperfusion
KW - Müller cell
KW - Retina
UR - http://www.scopus.com/inward/record.url?scp=17144426088&partnerID=8YFLogxK
U2 - 10.1002/glia.20151
DO - 10.1002/glia.20151
M3 - ???researchoutput.researchoutputtypes.contributiontojournal.article???
C2 - 15593100
AN - SCOPUS:17144426088
SN - 0894-1491
VL - 50
SP - 1
EP - 11
JO - GLIA
JF - GLIA
IS - 1
ER -