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Andreas Bringmann, Mike Francke, Thomas Pannicke, Bernd Biedermann, Frank Faude, Volker Enzmann, Peter Wiedemann, Winfried Reichelt, Andreas Reichenbach; Human Müller Glial Cells: Altered Potassium Channel Activity in Proliferative Vitreoretinopathy. Invest. Ophthalmol. Vis. Sci. 1999;40(13):3316-3323.
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purpose. To determine differences of K+ channel activity between
Müller glial cells obtained from retinas of healthy human donors
and of patients with retinal detachment and proliferative
methods. Müller cells were enzymatically isolated from retinas of healthy
donors and from excised retinal pieces of patients. The whole-cell and
the cell-attached configurations of the patch-clamp technique were used
to characterize the current densities of different K+ channel types and the activity of single Ca2+-activated
K+ channels of big conductance (BK).
results. Cells from patients displayed a less negative mean membrane potential
(−52.8 mV) than cells from healthy donors (−80.6 mV). However, the
membrane potentials in cells from patients scattered largely between−
6 and −99 mV. The inwardly rectifying K+ permeability in
cells from patients was strongly reduced (0.3 pA/pF) when compared with
cells from healthy donors (6.0 pA/pF). At the resting membrane
potential, single BK channels displayed a higher mean activity (open
probability, P o, and channel current
amplitude) in cells from patients (P o: 0.30)
than in cells from healthy donors (P o:
0.03). The variations of BK current amplitudes were correlated with the
variations of the membrane potential.
conclusions. The dominant expression of inwardly rectifying channels in cells from
healthy donors is thought to support important glial cell functions
such as the spatial buffering of extracellular K+. The
downregulation of these channels and the less negative mean membrane
potential in cells from patients should impair spatial buffering
currents and neurotransmitter clearance. The increased activity of BK
channels may support the proliferative activity of gliotic cells via
feedback regulation of Ca2+ entry and membrane
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