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Human Müller Glial Cells: Altered Potassium Channel Activity in Proliferative Vitreoretinopathy

¹ From the Department of Neurophysiology, Paul Flechsig Institute of Brain Research, University of Leipzig, D–04109 Leipzig; and the ² Department of Ophthalmology, Eye Hospital, University of Leipzig, D–04103 Leipzig, FRG.

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 vitreoretinopathy.

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 potential.

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