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Genetic Inactivation of an Inwardly Rectifying Potassium Channel (Kir4.1 Subunit) in Mice: Phenotypic Impact in Retina

Kofuji, Paulo and Ceelen, Paul and Zahs, Kathleen R. and Surbeck, Leslie W. and Lester, Henry A. and Newman, Eric A. (2000) Genetic Inactivation of an Inwardly Rectifying Potassium Channel (Kir4.1 Subunit) in Mice: Phenotypic Impact in Retina. Journal of Neuroscience, 20 (15). pp. 5733-5740. ISSN 0270-6474. PMCID PMC2410027. https://resolver.caltech.edu/CaltechAUTHORS:20200612-132259782

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Abstract

The inwardly rectifying potassium channel Kir4.1 has been suggested to underlie the principal K⁺ conductance of mammalian Müller 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 −/−). Müller 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 Müller 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 −/− Müller cells compared with Kir4.1 +/+ cells. The slow PIII response of the light-evoked electroretinogram (ERG), which is generated by K⁺ fluxes through Müller 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 Müller glial cells. The highly regulated localization and the functional properties of Kir4.1 in Müller cells suggest the involvement of this channel in the regulation of extracellular K⁺ in the mouse retina.


Item Type:Article
Related URLs:
URLURL TypeDescription
https://doi.org/10.1523/jneurosci.20-15-05733.2000DOIArticle
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2410027/PubMed CentralArticle
ORCID:
AuthorORCID
Lester, Henry A.0000-0002-5470-5255
Additional Information:© 2000 Society for Neuroscience. Received April 4, 2000; revised May 12, 2000; accepted May 17, 2000. This work was supported by National Institute of Health Grants GM-29836, MH-49176, EY04077, EY10383, and EY12949. We thank S. Pease, M. Larabee, and T. Wu for expert technical help.
Funders:
Funding AgencyGrant Number
NIHGM-29836
NIHMH-49176
NIHEY04077
NIHEY10383
NIHEY12949
Issue or Number:15
PubMed Central ID:PMC2410027
Record Number:CaltechAUTHORS:20200612-132259782
Persistent URL:https://resolver.caltech.edu/CaltechAUTHORS:20200612-132259782
Official Citation: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 Journal of Neuroscience 1 August 2000, 20 (15) 5733-5740; DOI: 10.1523/JNEUROSCI.20-15-05733.2000
Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:103879
Collection:CaltechAUTHORS
Deposited By: George Porter
Deposited On:12 Jun 2020 21:00
Last Modified:12 Jun 2020 21:00

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