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Titolo:
Genetic inactivation of an inwardly rectifying potassium channel (Kir4.1 subunit) in mice: Phenotypic impact in retina
Autore:
Kofuji, P; Ceelen, P; Zahs, KR; Surbeck, LW; Lester, HA; Newman, EA;
Indirizzi:
Univ Minnesota, Dept Neurosci, Minneapolis, MN 55455 USA Univ Minnesota Minneapolis MN USA 55455 urosci, Minneapolis, MN 55455 USA Univ Minnesota, Dept Physiol, Minneapolis, MN 55455 USA Univ Minnesota Minneapolis MN USA 55455 hysiol, Minneapolis, MN 55455 USA CALTECH, Div Biol, Pasadena, CA 91125 USA CALTECH Pasadena CA USA 91125CALTECH, Div Biol, Pasadena, CA 91125 USA
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 15, volume: 20, anno: 2000,
pagine: 5733 - 5740
SICI:
0270-6474(20000801)20:15<5733:GIOAIR>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
MULLER GLIAL-CELLS; COCHLEAR STRIA VASCULARIS; SOURCE-DENSITY ANALYSIS; K+-CHANNEL; B-WAVE; RAT RETINA; PIGMENT EPITHELIUM; EXTRACELLULAR K+; K-AB-2 KIR4.1; ION CHANNELS;
Keywords:
Muller cell; inwardly rectifying potassium channel; Kir4.1; retina; null mouse; glia; electroretinogram; slow PIII response; b-wave; astrocyte;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Kofuji, P Univ Minnesota, Dept Neurosci, 6-145 Jackson Hall,321 Church St SE, Minneapolis, MN 55455 USA Univ Minnesota 6-145 Jackson Hall,321 Church St SE Minneapolis MN USA 55455
Citazione:
P. Kofuji et al., "Genetic inactivation of an inwardly rectifying potassium channel (Kir4.1 subunit) in mice: Phenotypic impact in retina", J NEUROSC, 20(15), 2000, pp. 5733-5740

Abstract

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 largedepolarization of Kir4.1 -/- Muller cells compared with Kir4.1 +/+ cells. The slow PIII 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 Kin the mouse retina.

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Documento generato il 03/04/20 alle ore 20:03:30