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Characteristics of Müller glial cells in MNU-induced retinal degeneration

Published online by Cambridge University Press:  17 October 2016

MIRIAM REISENHOFER
Affiliation:
Department of Ophthalmology, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland Paul Flechsig Institute of Brain Research, Medical Faculty, University of Leipzig, 04103 Leipzig, Germany Department of Clinical Research, University of Bern, 3008 Bern, Switzerland
THOMAS PANNICKE
Affiliation:
Paul Flechsig Institute of Brain Research, Medical Faculty, University of Leipzig, 04103 Leipzig, Germany
ANDREAS REICHENBACH
Affiliation:
Paul Flechsig Institute of Brain Research, Medical Faculty, University of Leipzig, 04103 Leipzig, Germany
VOLKER ENZMANN*
Affiliation:
Department of Ophthalmology, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland Department of Clinical Research, University of Bern, 3008 Bern, Switzerland
*
*Address correspondence to: Volker Enzmann, Department of Ophthalmology, Inselspital, Bern University Hospital, Freiburgstr. 14, 3010 Bern, Switzerland. E-mail: [email protected]

Abstract

Retinal Müller glial cells have been shown to undergo reactive gliosis in a variety of retinal diseases. Upregulation of glial fibrillary acidic protein (GFAP) is a hallmark of Müller cell activation. Reactive gliosis after retinal detachment or ischemia/reperfusion is characterized by hypertrophy and downregulation of inwardly rectifying K+ (Kir) currents. However, this kind of physiological alteration could not be detected in slowly progressing retinal degenerations. The photoreceptor toxin N-methyl-N-nitrosourea (MNU) leads to the rapid loss of cells in the outer nuclear layer and subsequent Müller cell activation. Here, we investigated whether Müller cells from MNU-treated mice exhibit reactive gliosis. We found that Müller cells showed increased GFAP expression and increased membrane capacitance, indicating hypertrophy. Membrane potential and Kir channel-mediated K+ currents were not significantly altered whereas Kir4.1 mRNA expression and Kir-mediated inward current densities were markedly decreased. This suggests that MNU-induced Müller cell gliosis is characterized by plasma membrane increase without alteration in the membrane content of Kir channels. Taken together, our findings show that Müller cells of MNU-treated mice are reactive and respond with a form of gliosis which is characterized by cellular hypertrophy but no changes in Kir current amplitudes.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2016 

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