Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Kofuji, P. et al.

Kofuji, Ceelen, Zahs, Surbeck, Lester, Newman,

Genetic inactivation of an inwardly rectifying potassium channel (Kir4.1 subunit) in mice: phenotypic impact in retina.

The inwardly rectifying potassium channel Kir4.1 has been suggested to underlie the principal K(+) conductance of mammalian MÃ¼ller 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 -/-). MÃ¼ller 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 MÃ¼ller 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 -/- MÃ¼ller cells compared with Kir4.1 +/+ cells. The slow PIII response of the light-evoked electroretinogram (ERG), which is generated by K(+) fluxes through MÃ¼ller 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 MÃ¼ller glial cells. The highly regulated localization and the functional properties of Kir4.1 in MÃ¼ller cells suggest the involvement of this channel in the regulation of extracellular K(+) in the mouse retina.[1]

References

Genetic inactivation of an inwardly rectifying potassium channel (Kir4.1 subunit) in mice: phenotypic impact in retina. Kofuji, P., Ceelen, P., Zahs, K.R., Surbeck, L.W., Lester, H.A., Newman, E.A. J. Neurosci. (2000) [Pubmed]

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