Loss of inwardly rectifying potassium currents by human retinal glial cells in diseases of the eye

We compared the inward K+ currents of Müller glial cells from healthy and pathologically changed human retinas. To this purpose, the whole‐cell voltage‐clamp technique was performed on noncultured Müller cells acutely isolated from human retinas. Cells originated from retinas of four healthy organ d...

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Published in:Glia 1997-07, Vol.20 (3), p.210-218
Main Authors: Francke, Mike, Pannicke, Thomas, Biedermann, Bernd, Faude, Frank, Wiedemann, Peter, Reichenbach, Andreas, Reichelt, Winfried
Format: Article
Language:English
Subjects:
Barium - pharmacology
Biological and medical sciences
Eye Diseases - metabolism
glial cells
glutamate transport
Humans
In Vitro Techniques
K+ currents
Medical sciences
membrane potential
Membrane Potentials
Miscellaneous
Müller cells
Neuroglia - drug effects
Neuroglia - metabolism
Ophthalmology
Potassium - pharmacology
Potassium Channel Blockers
Potassium Channels - metabolism
Retina - metabolism
Retina - pathology
spatial buffering
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Summary:We compared the inward K+ currents of Müller glial cells from healthy and pathologically changed human retinas. To this purpose, the whole‐cell voltage‐clamp technique was performed on noncultured Müller 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. Müller cells from organ donors displayed inward K+ currents in the whole‐cell mode similar to those found in other species. In contrast, this pattern was clearly changed in the Müller cells from patient retinas. In whole‐cell recordings many Müller cells had strongly decreased inward K+ current amplitudes or lost these currents completely. Thus, the mean input resistance of Müller cells from patients was significantly increased to 1,129 ± 812 MΩ, compared to 279 ± 174 MΩ in Müller cells from healthy organ donor retinas. Accordingly, since the membrane potential is mainly determined by the K+ inward conductance in healthy Müller cells, a large amount of Müller cells from patient retinas had a membrane potential which was significantly lower than that of Müller cells from control eyes. The mean membrane potentials were −37 ± 24 mV and −63 ± 25 mV for patient and donor Müller cells, respectively. The newly described membrane characteristic changes of Müller cells from patient eyes are assumed to interfere severely with normal retinal function: (1) the retinal K+ homeostasis, which is partly regulated by the Müller cell‐mediated spatial buffering, should be disturbed, and (2) the diminished membrane potential should influence voltage‐dependent transporter systems of the Müller cells, e.g., the Na+‐dependent glutamate uptake. GLIA 20:210–218, 1997. © 1997 Wiley‐Liss, Inc.
ISSN:0894-1491
1098-1136
DOI:10.1002/(SICI)1098-1136(199707)20:3<210::AID-GLIA5>3.0.CO;2-B