Abstract

DO.09.02

Role of potassium channels in Müller cells

Serguei N. Skatchkov

Department of Biochemistry, Universidad Central del Caribe, School of Medicine, Bayamón, PR

Purpose
A high membrane potential is relevant for different functional roles of Müller cells, e.g. glutamate uptake, and retinal potassium and osmohomeostasis. The membrane potential of Müller cells is maintained by the activity of inwardly rectifying potassium (Kir) channels (e.g. Kir4.1) and two-pore domain (2P) TASK-1 channels (Glia 2002;38:256; Glia 2006;53:266). Disturbances in the glutamate, osmo-, and potassium homeostasis can be observed when Kir4.1 channels in glial cells are inactivated by siRNA (Glia 2007;55:274), conditional knockout (J Neurosci 2007;27:11354), ischemia (Glia 2005;50:1) or diabetes (Diabetes 2006;55:633). It is known that the potassium currents of Müller cells decrease after transient retinal ischemia which is associated with a depolarization of the cells (Mol Cell Neurosci 2004;26:493). Here we investigated whether the membrane potential and potassium currents of Müller cells may recover when pressure induced transient retinal ischemia is moderate.
Methods
The intraocular pressure in rat eyes was experimentally elevated above the systolic pressure for less than 1 hour. Thereafter, the membrane potential and potassium currents were recorded in isolated Müller cells by using patch clamp techniques.
Results
We found that the membrane potential of Müller cells decreased from -82±3 mV (control) to -51±9 mV 2-4 days after transient retinal ischemia. However, the potential restored to -73±8 mV 7-10 days after ischemia (~90% recovery). The inward potassium currents in Müller cells were strongly depressed from 2.3±0.5 nA (control) to 0.5±0.3 nA 2-4 days after ischemia, and restored to 1.3±0.5 nA 7-10 days after ischemia. Recovery of inward currents was only ~51% of control.
Conclusion
The results demonstrate that glia-specific potassium channels are depressed after retinal trauma, but may recover their function in longer time periods. This may be relevant to understanding glaucoma-related disorders. The recovery of the membrane potential despite no comparable recovery of inward currents suggests that 2P outwardly rectifying channels may be responsible.
Support
NIMGS-MBRS-SO6-GM50695, NIH-NCRR-RCMI-G12RR03035, NIH-NINDS-S11-NS48201, NIH-NINDS and NCRR SNRP-NS39408.

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