ATP-evoked calcium responses of radial glial (Müller) cells in the postnatal rabbit retina

2002 ◽  
Vol 70 (2) ◽  
pp. 209-218 ◽  
Author(s):  
Ortrud Uckermann ◽  
Jens Grosche ◽  
Andreas Reichenbach ◽  
Andreas Bringmann
Keyword(s):  
Müller Cells ◽  
Rabbit Retina ◽  
Muller Cells ◽  
Radial Glial

Na+,K+-activated adenosine triphosphatase of isolated Müller cells from the rabbit retina shows a K+ dependence similar to that of brain astrocytes

1985 ◽  
Vol 59 (3) ◽  
pp. 281-284 ◽  
Author(s):  
Andreas Reichenbach ◽  
Dietrich Dettmer ◽  
Winfried Reichelt ◽  
Wolfgang Eberhardt
Keyword(s):  
Adenosine Triphosphatase ◽  
Müller Cells ◽  
Rabbit Retina ◽  
Muller Cells

Rabbit retinal neurons and glia express a variety of ENaC/DEG subunits

2002 ◽  
Vol 283 (1) ◽  
pp. C126-C134 ◽  
Author(s):  
L. M. Brockway ◽  
Z.-H. Zhou ◽  
J. K. Bubien ◽  
B. Jovov ◽  
D. J. Benos ◽  
...  
Keyword(s):  
Expression Patterns ◽  
Müller Cells ◽  
Immunohistochemical Localization ◽  
Mammalian Brain ◽  
Rabbit Retina ◽  
Muller Cells ◽  
Retinal Neurons ◽  
Cellular Expression ◽  
The Central Nervous System ◽  
First Time

Some members of the epithelial Na+ channel/degenerin (ENaC/DEG) family of ion channels have been detected in mammalian brain. Therefore, we examined the RNA and protein expression of these channels in another part of the central nervous system, the rabbit retina. We next sought to demonstrate physiological evidence for an amiloride-sensitive current in Müller glia, which, on the basis of a previous study, are thought to express α-ENaC (Golestaneh N, de Kozak Y, Klein C, and Mirshahi M. Glia 33: 160–168, 2001). RT-PCR of retinal RNA revealed the presence of α-, β-, γ-, and δ-ENaC as well as acid-sensing ion channel (ASIC)1, ASIC2, ASIC3, and ASIC4. Immunohistochemical localization with antibodies against α-ENaC and β-ENaC showed labeling in Müller cells and neurons, respectively. The presence of α-ENaC, β-ENaC, and ASIC1 was detected by Western blotting. Cultured Müller cells were whole cell patch clamped. These cells exhibited an inward Na+ current that was blocked by amiloride. These data demonstrate for the first time both the expression of a variety of ENaC and ASIC subunits in the rabbit retina as well as distinct cellular expression patterns of specific subunits in neurons and glia.

Development of the rabbit retina: II. Müller cells

1991 ◽  
Vol 311 (1) ◽  
pp. 33-44 ◽  
Author(s):  
A. Reichenbach ◽  
J. Schnitzer ◽  
A. Friedrich ◽  
A.-K. Knothe ◽  
A. Henke
Keyword(s):  
Müller Cells ◽  
Rabbit Retina ◽  
Muller Cells

scholarly journals Review and Hypothesis: A Potential Common Link Between Glial Cells, Calcium Changes, Modulation of Synaptic Transmission, Spreading Depression, Migraine, and Epilepsy—H+

2021 ◽  
Vol 15 ◽  
Author(s):  
Robert Paul Malchow ◽  
Boriana K. Tchernookova ◽  
Ji-in Vivien Choi ◽  
Peter J. S. Smith ◽  
Richard H. Kramer ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Intracellular Calcium ◽  
Glial Cells ◽  
Spreading Depression ◽  
Müller Cells ◽  
Extracellular Atp ◽  
Muller Cells ◽  
Radial Glial Cells ◽  
Synaptic Modulation ◽  
Radial Glial

There is significant evidence to support the notion that glial cells can modulate the strength of synaptic connections between nerve cells, and it has further been suggested that alterations in intracellular calcium are likely to play a key role in this process. However, the molecular mechanism(s) by which glial cells modulate neuronal signaling remains contentiously debated. Recent experiments have suggested that alterations in extracellular H+ efflux initiated by extracellular ATP may play a key role in the modulation of synaptic strength by radial glial cells in the retina and astrocytes throughout the brain. ATP-elicited alterations in H+ flux from radial glial cells were first detected from Müller cells enzymatically dissociated from the retina of tiger salamander using self-referencing H+-selective microelectrodes. The ATP-elicited alteration in H+ efflux was further found to be highly evolutionarily conserved, extending to Müller cells isolated from species as diverse as lamprey, skate, rat, mouse, monkey and human. More recently, self-referencing H+-selective electrodes have been used to detect ATP-elicited alterations in H+ efflux around individual mammalian astrocytes from the cortex and hippocampus. Tied to increases in intracellular calcium, these ATP-induced extracellular acidifications are well-positioned to be key mediators of synaptic modulation. In this article, we examine the evidence supporting H+ as a key modulator of neurotransmission, review data showing that extracellular ATP elicits an increase in H+ efflux from glial cells, and describe the potential signal transduction pathways involved in glial cell—mediated H+ efflux. We then examine the potential role that extracellular H+ released by glia might play in regulating synaptic transmission within the vertebrate retina, and then expand the focus to discuss potential roles in spreading depression, migraine, epilepsy, and alterations in brain rhythms, and suggest that alterations in extracellular H+ may be a unifying feature linking these disparate phenomena.

Developmental Regulation of Calcium Channel-Mediated Currents in Retinal Glial (Müller) Cells

2000 ◽  
Vol 84 (6) ◽  
pp. 2975-2983 ◽  
Author(s):  
A. Bringmann ◽  
S. Schopf ◽  
A. Reichenbach
Keyword(s):  
Glial Cells ◽  
Low Voltage ◽  
Developmental Regulation ◽  
Müller Cells ◽  
Cell Voltage ◽  
Charge Carriers ◽  
Muller Cells ◽  
Isolated Cells ◽  
Radial Glial Cells ◽  
Radial Glial

Whole cell voltage-clamp recordings of freshly isolated cells were used to study changes in the currents through voltage-gated Ca2+ channels during the postnatal development of immature radial glial cells into Müller cells of the rabbit retina. Using Ba2+ or Ca2+ ions as charge carriers, currents through transient low-voltage-activated (LVA) Ca2+ channels were recorded in cells from early postnatal stages, with an activation threshold at −60 mV and a peak current at −25 mV. To increase the amplitude of currents through Ca2+ channels, Na+ ions were used as the main charge carriers, and currents were recorded in divalent cation-free bath solutions. Currents through transient LVA Ca2+ channels were found in all radial glial cells from retinae between postnatal days 2 and 37. The currents activated at potentials positive to −80 mV and displayed a maximum at −40 mV. The amplitude of LVA currents increased during the first postnatal week; after postnatal day 6, the amplitude remained virtually constant. The density of LVA currents was highest at early postnatal days (days 2–5: 13 pA/pF) and decreased to a stable, moderate level within the first three postnatal weeks (3 pA/pF). A significant expression of currents through sustained, high-voltage-activated Ca2+ channels was found after the third postnatal week in ∼25% of the investigated cells. The early and sole expression of transient currents at high-density may suggest that LVA Ca2+ channels are involved in early developmental processes of rabbit Müller cells.

K+ Channels of Müller Glial Cells in Retinal Disorders

2018 ◽  
Vol 17 (4) ◽  
pp. 255-260 ◽  
Author(s):  
Feng Gao ◽  
Lin-Jie Xu ◽  
Yuan Zhao ◽  
Xing-Huai Sun ◽  
Zhongfeng Wang
Keyword(s):  
Müller Cells ◽  
Major Type ◽  
Delayed Rectifier ◽  
Muller Cells ◽  
Bkca Channels ◽  
K Channels ◽  
Functional Changes ◽  
Physiological Properties ◽  
Retinal Disorders ◽  
Inwardly Rectifying

Background & Objective: Müller cell is the major type of glial cell in the vertebrate retina. Müller cells express various types of K+ channels, such as inwardly rectifying K+ (Kir) channels, big conductance Ca2+-activated K+ (BKCa) channels, delayed rectifier K+ channels (KDR), and transient A-type K+ channels. These K+ channels play important roles in maintaining physiological functions of Müller cells. Under some retinal pathological conditions, the changed expression and functions of K+ channels may contribute to retinal pathogenesis. Conclusion: In this article, we reviewed the physiological properties of K+ channels in retinal Müller cells and the functional changes of these channels in retinal disorders.

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