In the retina of most vertebrates there exists only one type of macroglia, the Müller cell. Müller cells express voltage-gated ion channels, neurotransmitter receptors and various uptake carrier systems. These properties enable the Müller cells to control the activity of retinal neurons by regulating the extracellular concentration of neuroactive substances such as K+
, GABA and glutamate. We show here how electrophysiological recordings from enzymatically dissociated mammalian Müller cells can be used to study these mechanisms. Müller cells from various species have Na+
-dependent GABA uptake carriers, but only cells from primates have additional GABA receptors that activate Cl––
channels. Application of glutamate analogues causes enhanced membrane currents recorded from Müller cells in situ but not from isolated cells. We show that mammalian Müller cells have no ionotropic glutamate receptors but respond to increased K+
release from glutamate-stimulated retinal neurons. This response is involved in extracellular K+
clearance and is mediated by voltagegated (inwardly rectifying) K+
channels which are abundantly expressed by healthy Müller cells. In various cases of human retinal pathology, currents through these channels are strongly reduced or even extinguished. Another type of voltagegated ion channels, observed in Müller cells from many mammalian species, are Na+
channels. In Müller cells from diseased human retinae, voltage-dependent Na+
currents were significantly increased in comparison to cells from control donors. Thus, the expression of glial ion channels seems to be controlled by neuronal signals. This interaction may be involved in the pathogenesis of retinal gliosis which inevitably accompanies any degeneration of retinal neurons. In particular, Müller cell proliferation may be triggered by mechanisms requiring the activation of Ca2+
currents are easily elicitable in Müller cells from degenerating retinae and can be blocked by 1 mM
TEA (tetraethylammonium). In purified Müller cell cultures, the application of 1 mM
TEA greatly reduces the proliferative activity of the cells. These data clearly show that Müller cells are altered in cases of neuronal degeneration and may be crucially involved in pathogenetic mechanisms of the retina.
Prof. Andreas Reichenbach, Paul-Flechsig-Institut Für Hirnforschung, Abteilung Neurophysiologie, Universität Leipzig, Jahnallee 59, D-04109 Leipzig (Germany), Tel. 341 9725731, Fax 341 9725739, E-Mail firstname.lastname@example.org
Published online: December 11, 2009
Number of Print Pages : 15
Ophthalmic Research (Journal for Research in Experimental and Clinical Ophthalmology)
Vol. 29, No. 5, Year 1997 (Cover Date: 1997)
Journal Editor: Pleyer U. (Berlin)
ISSN: 0030-3747 (Print), eISSN: 1423-0259 (Online)
For additional information: http://www.karger.com/ORE
Copyright / Drug Dosage
Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.