## 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 (
Electrophysiological properties of rat retinal Müller (glial) cells in postnatally developing and in pathologically altered retinae
✍ Scribed by Felix Felmy; Thomas Pannicke; Jürgen A. Richt; Andreas Reichenbach; Elke Guenther
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- English
- Weight
- 372 KB
- Volume
- 34
- Category
- Article
- ISSN
- 0894-1491
No coin nor oath required. For personal study only.
✦ Synopsis
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 rat Müller cells is less well studied. The aim of the present study was to characterize their membrane currents in postnatal development and in two models of retinal degeneration. Freshly isolated cells were subjected to whole‐cell patch clamp recordings. During the first 4 weeks after birth of rats, their Müller cells displayed an increase in all membrane currents, particularly in the inward currents elicited at hyperpolarizing potentials. The decrease of the membrane resistance from more than 760 MΩ to less than 50 MΩ was accompanied by a shift of the zero current potential from about −20 mV to −80 mV, similar as earlier observed in developing rabbit Müller cells. These developmental changes were found in pigmented Brown Norway rats as well as in rats with inherited retinal dystrophy (RCS rats). Moreover, an infection of Lewis rats with the Borna disease virus caused substantial neuroretinal degeneration but did not result in a strong reduction of inward currents and of the zero current potential of the Müller cells. Thus, rat Müller cells fail to change their basic membrane properties in two different models of retinal pathology. This is in contrast to human and rabbit Müller cells, which have been shown to undergo dramatic changes of their membrane physiology in response to retinal diseases and injuries. GLIA 34:190–199, 2001. © 2001 Wiley‐Liss, Inc.
📜 SIMILAR VOLUMES
## Abstract The electrophysiology of murine Müller cells, and of their precursors, during postnatal development was investigated by using the whole‐cell patch‐clamp technique. Membrane potential, membrane capacitance, and expression of voltage‐gated Na^+^ currents increased during the first 3 postn
Inwardly rectifying K+ (Kir) channels have been implicated in the mediation of retinal K+ homeostasis by Muller glial cells. To assess possible involvement of altered glial K+ channel expression in ischemia-reperfusion injury, transient retinal ischemia was induced in rat eyes. Acutely isolated Mull
## Abstract Infection with the neurotropic Borna disease virus (BDV) causes an immune‐mediated neurological disease in a broad range of species. In addition to encephalitis, BDV‐infected Lewis rats develop a retinitis histologically characterized by the loss of most retinal neurons. By contrast, th
## Abstract Here we show that rabbit Müller cell differentiation from radial glial progenitor cells is accompanied by a decreasing capability to respond to specific stimuli (depolarization and extracellular adenosine 5′‐triphosphate [ATP]) with an elevation of intracellular calcium. Intracellular f
## Abstract Cryosection of an embryonic day 12.5 eye labeled for Sox9 (orange), Pax6 (blue), and DAPI (purple). J. Comp. Neurol. 510:237–250, 2008. © 2008 Wiley‐Liss, Inc.