Loss of inwardly rectifying potassium currents by human retinal glial cells in diseases of the eye
✍ Scribed by Mike Francke; Thomas Pannicke; Bernd Biedermann; Frank Faude; Peter Wiedemann; Andreas Reichenbach; Winfried Reichelt
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 166 KB
- Volume
- 20
- Category
- Article
- ISSN
- 0894-1491
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✦ Synopsis
We compared the inward K 1 currents of Mu ¨ller glial cells from healthy and pathologically changed human retinas. To this purpose, the whole-cell voltage-clamp technique was performed on noncultured Mu ¨ller cells acutely isolated from human retinas. Cells originated from retinas of four healthy organ donors and of 24 patients suffering from different vitreoretinal and chorioretinal diseases. Mu ¨ller cells from organ donors displayed inward K 1 currents in the whole-cell mode similar to those found in other species. In contrast, this pattern was clearly changed in the Mu ¨ller cells from patient retinas. In whole-cell recordings many Mu ¨ller cells had strongly decreased inward K 1 current amplitudes or lost these currents completely. Thus, the mean input resistance of Mu ¨ller cells from patients was significantly increased to 1,129 6 812 MV, compared to 279 6 174 MV in Mu ¨ller cells from healthy organ donor retinas. Accordingly, since the membrane potential is mainly determined by the K 1 inward conductance in healthy Mu ¨ller cells, a large amount of Mu ¨ller cells from patient retinas had a membrane potential which was significantly lower than that of Mu ¨ller cells from control eyes. The mean membrane potentials were 237 6 24 mV and 263 6 25 mV for patient and donor Mu ¨ller cells, respectively. The newly described membrane characteristic changes of Mu ¨ller cells from patient eyes are assumed to interfere severely with normal retinal function: (1) the retinal K 1 homeostasis, which is partly regulated by the Mu ¨ller cell-mediated spatial buffering, should be disturbed, and (2) the diminished membrane potential should influence voltage-dependent transporter systems of the Mu ¨ller cells, e.g., the Na 1 -dependent glutamate uptake.