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1 From the Paul Flechsig Institute for Brain Research and the 2 Department of Ophthalmology, Eye Hospital, University of Leipzig, Germany.
PURPOSE. To determine the electrophysiological properties of Müller (glial) cells from experimentally detached rabbit retinas.
METHODS. A stable local retinal detachment was induced by subretinal injection of a sodium hyaluronate solution. Müller cells were acutely dissociated and studied by the whole-cell voltage-clamp technique.
RESULTS. The cell membranes of Müller cells from normal retinas were
dominated by a large inwardly rectifying potassium ion (K+)
conductance that caused a low-input resistance (<100 M
) and a high
resting membrane potential (-82 ± 6 mV). During the first week
after detachment, the Müller cells became reactive as shown by
glial fibrillary acidic protein (GFAP) immunoreactivity, and their
inward currents were markedly reduced, accompanied by an increased
input resistance (>200 M). After 3 weeks of detachment, the input
resistance increased further (>300 M), and some cells displayed
significantly depolarized membrane potentials (mean -69 ± 18
mV). When PVR developed (in 20% of the cases) the inward
K+ currents were virtually completely eliminated. The input
resistance increased dramatically (>1000 M), and almost all cells
displayed strongly depolarized membrane potentials (-44 ± 16
mV).
CONCLUSIONS. Reactive Müller cells are characterized by a severe reduction of their K+ inward conductance, accompanied by depolarized membrane potentials. These changes must impair physiological glial functions, such as neurotransmitter recycling and K+ ion clearance. Furthermore, the open probability of certain types of voltage-dependent ion channels (e.g., Ca2+-dependent K+ maxi channels) increases that may be a precondition for Müller cell proliferation, particularly in PVR when a dramatic downregulation of both inward current density and resting membrane potential occurs.
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