Original Article

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

  1. Thomas Pannicke1,*,
  2. Ortrud Uckermann1,
  3. Ianors Iandiev1,
  4. Bernd Biedermann1,
  5. Peter Wiedemann2,
  6. Ido Perlman3,
  7. Andreas Reichenbach1,
  8. Andreas Bringmann2

Article first published online: 8 DEC 2004

DOI: 10.1002/glia.20151

Issue

Glia

Glia

Volume 50, Issue 1, pages 1–11, 1 April 2005

Additional Information

How to Cite

Pannicke, T., Uckermann, O., Iandiev, I., Biedermann, B., Wiedemann, P., Perlman, I., Reichenbach, A. and Bringmann, A. (2005), Altered membrane physiology in Müller glial cells after transient ischemia of the rat retina. Glia, 50: 1–11. doi: 10.1002/glia.20151

Author Information

  1. 1

    Paul-Flechsig-Institut für Hirnforschung, Abteilung Neurophysiologie, Universität Leipzig, Leipzig, Germany

  2. 2

    Klinik und Poliklinik für Augenheilkunde, Universität Leipzig, Leipzig, Germany

  3. 3

    Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel

*Paul-Flechsig-Institut für Hirnforschung, Universität Leipzig, Jahnallee 59, D-04109 Leipzig, Germany

Publication History

  1. Issue published online: 7 FEB 2005
  2. Article first published online: 8 DEC 2004
  3. Manuscript Accepted: 6 OCT 2004
  4. Manuscript Received: 26 APR 2004

Funded by

  • Bundesministerium für Bildung, Forschung und Technologie, Interdisciplinary Center for Clinical Research at the University of Leipzig. Grant Number: 01KS9504 (Project C21)
  • Deutsche Forschungsgemeinschaft. Grant Number: BR1249/2-1

SEARCH

SEARCH BY CITATION

ARTICLE TOOLS

View Full Article (HTML) Get PDF (285K)

Keywords:

  • Müller cell;
  • glia;
  • inwardly rectifying potassium channel;
  • ischemia-reperfusion;
  • retina

Abstract

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. © 2004 Wiley-Liss, Inc.

View Full Article (HTML) Get PDF (285K)