title: 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.
authors.affiliation: Paul-Flechsig-Institut für Hirnforschung, Abteilung Neurophysiologie, Universität Leipzig, Leipzig, Germany. pant@medizin.uni-leipzig.de
authors.forename: Thomas
authors.initials: T
authors.lastname: Pannicke
authors.forename: Ortrud
authors.initials: O
authors.lastname: Uckermann
authors.forename: Ianors
authors.initials: I
authors.lastname: Iandiev
authors.forename: Bernd
authors.initials: B
authors.lastname: Biedermann
authors.forename: Peter
authors.initials: P
authors.lastname: Wiedemann
authors.forename: Ido
authors.initials: I
authors.lastname: Perlman
authors.forename: Andreas
authors.initials: A
authors.lastname: Reichenbach
authors.forename: Andreas
authors.initials: A
authors.lastname: Bringmann
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism / Q000503:physiopathology; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism*; D002478:Cells, Cultured; D015536:Down-Regulation / Q000187:drug effects / Q000502:physiology; D005260:Female; D018698:Glutamic Acid / Q000378:metabolism / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009410:Nerve Degeneration / Q000378:metabolism / Q000503:physiopathology; D009457:Neuroglia / Q000187:drug effects / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000378:metabolism; D024661:Potassium Channels, Inwardly Rectifying / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D020318:Rats, Long-Evans; D015427:Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology; D012160:Retina / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D012164:Retinal Diseases / Q000378:metabolism / Q000503:physiopathology; D015222:Sodium Channels / Q000378:metabolism
chemical_list: D024661:Potassium Channels, Inwardly Rectifying; D015222:Sodium Channels; D018698:Glutamic Acid; D011188:Potassium