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Retinal Detachment Model in Rodents by Subretinal Injection of Sodium Hyaluronate
Published on: September 11, 2013
Electrophysiology of rabbit Müller (glial) cells in experimental retinal detachment and PVR
M Francke1, F Faude, T Pannicke
1Paul Flechsig Institute for Brain Research and the. 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(Omega)) 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(Omega)). After 3 weeks of detachment, the input resistance increased further (>300 M(Omega)), 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 MOmega), 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.
Insights
Retinal detachment alters Müller glial cells, reducing potassium currents and depolarizing membranes. These changes impair essential glial functions and may promote cell proliferation, especially in proliferative vitreoretinopathy (PVR).
Area of Science:
- Neuroscience
- Ophthalmology
- Cell Biology
Background:
- Müller cells are crucial glial cells in the retina, maintaining its homeostasis.
- Retinal detachment triggers reactive changes in Müller cells, impacting their function.
Purpose of the Study:
- To investigate the electrophysiological properties of Müller cells in experimentally detached rabbit retinas.
- To understand how retinal detachment affects Müller cell ion channel activity and membrane potential.
Main Methods:
- Induction of local retinal detachment using subretinal injection of sodium hyaluronate in rabbits.
- Acute dissociation of Müller cells followed by whole-cell voltage-clamp recordings.
Main Results:
- Normal Müller cells exhibit high inward potassium (K+) conductance and hyperpolarized resting potentials.
- Following detachment, Müller cells showed reduced K+ conductance, increased input resistance, and depolarized membrane potentials.
- In cases of proliferative vitreoretinopathy (PVR), K+ currents were nearly eliminated, with dramatically increased resistance and severe depolarization.
Conclusions:
- Reactive Müller cells display significantly reduced K+ inward conductance and depolarized membrane potentials.
- These electrophysiological alterations likely impair vital glial functions, including neurotransmitter recycling and K+ ion clearance.
- Changes in ion channel activity may predispose Müller cells to proliferation, particularly in PVR.
