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Miriam Reisenhofer, Thomas Pannicke, Andreas Reichenbach, Volker Enzmann; Electrophysiological properties of Müller cells in MNU-induced retinal degeneration. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):4254.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Müller cells, the macroglia of the retina, are responsible for maintaining retinal ion and water homeostasis. Under certain pathological conditions, Müller cells become reactive and show decreased potassium currents. Here, we want to investigate whether Müller cells change their electrophysiological properties after MNU-induced retinal degeneration.
Adult C57BL/6 mice were treated with 60 mg/kg N-methyl-N-nitrosourea (MNU) and sacrificed 1, 3, 5 and 7 days post injection (PI). Whole cell patch clamp recordings were performed to determine membrane potential, cell capacitance and current amplitude. Quantitative real-time PCR (qPCR) was employed to quantify relative gene expression of the potassium channel subunit Kir4.1. Additionally, expression of Kir4.1 and Müller cell-specific markers (CRALBP, GFAP) was assessed by immunohistochemistry (IHC).
After MNU-treatment, Müller cells became reactive and displayed enhanced expression of the filament protein GFAP. Electrophysiological recordings showed unaltered membrane potential and currents. In contrast, membrane capacitance and current density were significantly increased or decreased, respectively. qPCR revealed significantly reduced Kir4.1 mRNA levels. However, protein expression of Kir4.1 was not changed.
In MNU-induced retinal degeneration, membrane potential and currents remained unaltered. Nevertheless, the increased membrane capacitances suggest an increase of the membrane surface typical for hypertrophy of reactive glial cells. The decrease of current densities suggests that the new membrane areas contain less membrane channels. Therefore, characteristics of Müller cell reactivity and gliosis will be subject to further investigations in the MNU model.
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