## Abstract Retinal glial Müller cells are characterized by dominant K^+^ conductances. The cells may undergo changes of their membrane currents during ontogeny and gliosis as described in rabbit and man. Although the rat retina is often used in physiological experiments, the electrophysiology of r
Electrophysiological properties of retinal Müller glial cells from myelin mutant rat
✍ Scribed by Andrés E. Chávez; Thomas Pannicke; Manuel Roncagliolo; Andreas Reichenbach; Adrián G. Palacios
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 415 KB
- Volume
- 45
- Category
- Article
- ISSN
- 0894-1491
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✦ Synopsis
Abstract
The structural and functional similarities between Müller cells and oligodendrocytes prompted the present study of the electrophysiological properties of Müller (glia) cells obtained from the retinae of control and myelin mutant taiep rats during the postnatal developmental period (P12–P180). The whole‐cell configuration of the patch‐clamp technique was used to characterize the general properties and the K^+^ currents from dissociated Müller cells. During the first 3 weeks of life, a decrease of the membrane resistance and an increase of the membrane potential were observed in Müller cells from both control and taiep rats. However, Müller cells from taiep rats never achieved the very negative membrane potential (−50 mV vs −80 mV) and the low membrane resistance characteristic for control cells. Furthermore, Müller cells displayed increased inward and outward K^+^ currents during postnatal development up to P30/60 in controls; however, in taiep rats, this increase ceased at P20/30, and low‐amplitude currents persisted into adulthood. These results provide first evidence of physiological changes in retinal Müller cells as a consequence of a myelin mutation causing a progressive deterioration of the central nervous system (CNS) due to a disturbance of the microtubule network of oligodendrocytes. We hypothesize that the progressive dysmyelination process of the optic nerve, accompanied by functional deficits of retinal neurons (e.g., ganglion cells), induces physiological alterations of Müller cells. © 2003 Wiley‐Liss, Inc.
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