| First Author | Connors NC | Year | 2002 |
| Journal | J Neurosci | Volume | 22 |
| Issue | 11 | Pages | 4321-7 |
| PubMed ID | 12040037 | Mgi Jnum | J:125566 |
| Mgi Id | MGI:3759166 | Doi | 10.1523/JNEUROSCI.22-11-04321.2002 |
| Citation | Connors NC, et al. (2002) Dystrophin Dp71 is critical for the clustered localization of potassium channels in retinal glial cells. J Neurosci 22(11):4321-7 |
| abstractText | The Muller cell is the principal glial cell of the vertebrate retina. The primary conductance in Muller cells is the inwardly rectifying potassium channel Kir4.1 (BIR10 and KAB-2), which is highly concentrated at the endfeet at the vitreal border and to processes enveloping blood vessels. Such asymmetric and clustered distribution of Kir4.1 channels in Muller cells is thought to be critical for the buffering of extracellular potassium concentration in retina. Herein we investigated whether the distribution and functional properties of Kir4.1 channels are dependent on expression of the Dp71, a dystrophin isoform expressed in Muller cells. Kir4.1 distribution was determined in mouse retinal sections and whole mounts using anti-Kir4.1 antibodies and confocal microscopy. In Muller cells from wild-type mice, Kir4.1 is highly clustered in their endfeet and perivascular processes. In contrast, in Muller cells from the mdx(3Cv) mouse, which lacks the expression of Dp71, the Kir4.1 immunoreactivity is evenly distributed throughout the cell membrane. Surface expression of Kir4.1 is not affected in mdx(3Cv) Muller cells as current density of barium-sensitive inward currents in mdx(3Cv) Muller cells are not different from wild type. Focal extracellular potassium increases in isolated Muller cells shows that Kir channels in the mdx(3Cv) cells, as opposed to wild type, are less prominently concentrated in their endfeet. In summary, our data indicate that Dp71 is critical for the clustering but not membrane expression of Kir4.1 in mouse Muller cells. These results point to a new role for dystrophin in glial cells. |
