Genetic inactivation of an inwardly rectifying potassium channel (kir4.1 Subunit) in mice: Phenotypic impact in retina

Paulo Kofuji, Paul Ceelen, Kathleen R. Zahs, Leslie W. Surbeck, Henry A. Lester, Eric A. Newman

Research output: Contribution to journalArticlepeer-review

402 Scopus citations


The inwardly rectifying potassium channel Kir4.1 has been suggested to underlie the principal K+ conductance of mammalian Muller cells and to participate in the generation of field potentials and regulation of extracellular K+ in the retina. To further assess the role of Kir4.1 in the retina, we generated a mouse line with targeted disruption of the Kir4.1 gene (Kir4.1 -/-). Muller cells from Kir4.1 -/- mice were not labeled with an anti-Kir4.1 antibody, although they appeared morphologically normal when stained with an anti-glutamine synthetase antibody. In contrast, in Muller cells from wild-type littermate (Kir4.1 +/+) mice, Kir4.1 was present and localized to the proximal endfeet and perivascular processes. In situ whole-cell patch-clamp recordings showed a 10-fold increase in the input resistance and a large depolarization of Kir4.1 -/- Muller cells compared with Kir4.1 +/+ cells. The slow PIll response of the light-evoked electroretinogram (ERG), which is generated by K+ fluxes through Muller cells, was totally absent in retinas from Kir4.1 -/- mice. The b-wave of the ERG, in contrast, was spared in the null mice. Overall, these results indicate that Kir4.1 is the principal K+ channel subunit expressed in mouse Muller glial cells. The highly regulated localization and the functional properties of Kir4.1 in Muller cells suggest the involvement of this channel in the regulation of extracellular K+ in the mouse retina.

Original languageEnglish (US)
Pages (from-to)5733-5740
Number of pages8
JournalJournal of Neuroscience
Issue number15
StatePublished - Aug 1 2000


  • Astrocyte
  • B-wave
  • Electroretinogram
  • Glia
  • Inwardly rectifying potassium channel
  • Kir4.1
  • Muller cell
  • Null mouse
  • Retina
  • Slow PIII response


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