High-voltage-activated calcium channels in Müller cells acutely isolated from tiger salamander retina

Glia ◽  
2004 ◽  
Vol 49 (2) ◽  
pp. 259-274 ◽  
Author(s):  
Nicole C. Welch ◽  
Stephanie Wood ◽  
Christine Jollimore ◽  
Kelly Stevens ◽  
Melanie E.M. Kelly ◽  
...  
Keyword(s):  
Calcium Channels ◽  
High Voltage ◽  
Müller Cells ◽  
Tiger Salamander ◽  
Muller Cells

Cannabinoid receptor agonists modulate calcium channels in rat retinal müller cells

Neuroscience ◽  
2016 ◽  
Vol 313 ◽  
pp. 213-224 ◽  
Author(s):  
W. Yang ◽  
Q. Li ◽  
S.-Y. Wang ◽  
F. Gao ◽  
W.-J. Qian ◽  
...  
Keyword(s):  
Calcium Channels ◽  
Cannabinoid Receptor ◽  
Müller Cells ◽  
Muller Cells ◽  
Receptor Agonists

ATP-mediated Increase in H+ Flux from Retinal Müller Cells: a Role for Na+/H+ Exchange

2020 ◽  
Author(s):  
Boriana K Tchernookova ◽  
Michael W Gongwer ◽  
Alexis George ◽  
Brock Goeglein ◽  
Alyssa M Powell ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Neurotransmitter Release ◽  
Müller Cells ◽  
Cell Voltage ◽  
Extracellular Atp ◽  
Extracellular Potassium ◽  
Tiger Salamander ◽  
Synaptic Connections ◽  
Muller Cells ◽  
Extracellular Sodium

Small alterations in extracellular H+ can profoundly alter neurotransmitter release by neurons. We examined mechanisms by which extracellular ATP induces an extracellular H+ flux from Müller glial cells, which surround synaptic connections throughout the vertebrate retina. Müller glia were isolated from tiger salamander retinae and H+ fluxes examined using self-referencing H+-selective microelectrodes. Experiments were performed in 1 mM HEPES with no bicarbonate present. Replacement of extracellular sodium by choline decreased H+ efflux induced by 10 µM ATP by 75%. ATP-induced H+ efflux was also reduced by Na+/H+ exchange inhibitors. Amiloride reduced H+ efflux initiated by 10 µM ATP by 60%, while 10 µM cariporide decreased by 37%, and 25 µM zoniporide reduced H+ flux by 32%. ATP-induced H+ fluxes were not significantly altered by the K+/H+ pump blockers SCH28080 or TAK438, and replacement of all extracellular chloride with gluconate was without effect on H+ fluxes. Recordings of ATP-induced H+ efflux from cells simultaneously whole-cell voltage-clamped revealed no effect of membrane potential from -70 mV to 0 mV. Restoration of extracellular potassium after cells were bathed in 0 mM potassium produced a transient alteration in ATP-dependent H+ efflux. The transient response to extracellular potassium occurred only when extracellular sodium was present and was abolished by 1 mM ouabain, suggesting alterations in sodium gradients mediated by Na+/K ATPase activity. Our data indicate that the majority of H+ efflux elicited by extracellular ATP from isolated Müller cells is mediated by Na+/H+ exchange.

Calcium-activated chloride channels in müller cells acutely isolated from tiger salamander retina

Glia ◽  
2005 ◽  
Vol 53 (1) ◽  
pp. 74-80 ◽  
Author(s):  
Nicole C. Welch ◽  
Melanie R. Lalonde ◽  
Steven Barnes ◽  
Melanie E.M. Kelly
Keyword(s):  
Chloride Channels ◽  
Müller Cells ◽  
Tiger Salamander ◽  
Muller Cells

Effect of electrical stimulation on IGF-1 transcription by L-type calcium channels in cultured retinal Müller cells

2008 ◽  
Vol 52 (3) ◽  
pp. 217-223 ◽  
Author(s):  
Tatsuhiko Sato ◽  
Takashi Fujikado ◽  
Takeshi Morimoto ◽  
Kenji Matsushita ◽  
Takayuki Harada ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Calcium Channels ◽  
Müller Cells ◽  
Muller Cells

scholarly journals Extracellular H+ fluxes from tiger salamander Müller (glial) cells measured using self-referencing H+-selective microelectrodes

2017 ◽  
Vol 118 (6) ◽  
pp. 3132-3143 ◽  
Author(s):  
Matthew A. Kreitzer ◽  
David Swygart ◽  
Meredith Osborn ◽  
Blair Skinner ◽  
Chad Heer ◽  
...  
Keyword(s):  
Glial Cells ◽  
Müller Cells ◽  
Bicarbonate Transport ◽  
Extracellular Potassium ◽  
Tiger Salamander ◽  
Muller Cells ◽  
Extracellular Acidification ◽  
Müller Glial Cells ◽  
Bicarbonate Transporter ◽  
Induced Changes

Self-referencing H+-selective electrodes were used to measure extracellular H+ fluxes from Müller (glial) cells isolated from the tiger salamander retina. A novel chamber enabled stable recordings using H+-selective microelectrodes in a self-referencing format using bicarbonate-based buffer solutions. A small basal H+ flux was observed from the end foot region of quiescent cells bathed in 24 mM bicarbonate-based solutions, and increasing extracellular potassium induced a dose-dependent increase in H+ flux. Barium at 6 mM also increased H+ flux. Potassium-induced extracellular acidifications were abolished when bicarbonate was replaced by 1 mM HEPES. The carbonic anhydrase antagonist benzolamide potentiated the potassium-induced extracellular acidification, while 300 μM DIDS, 300 μM SITS, and 30 μM S0859 significantly reduced the response. Potassium-induced extracellular acidifications persisted in solutions lacking extracellular calcium, although potassium-induced changes in intracellular calcium monitored with Oregon Green were abolished. Exchange of external sodium with choline also eliminated the potassium-induced extracellular acidification. Removal of extracellular sodium by itself induced a transient alkalinization, and replacement of sodium induced a transient acidification, both of which were blocked by 300 μM DIDS. Recordings at the apical portion of the cell showed smaller potassium-induced extracellular H+ fluxes, and removal of the end foot region further decreased the H+ flux, suggesting that the end foot was the major source of acidifications. These studies demonstrate that self-referencing H+-selective electrodes can be used to monitor H+ fluxes from retinal Müller cells in bicarbonate-based solutions and confirm the presence of a sodium-coupled bicarbonate transporter, the activity of which is largely restricted to the end foot of the cell. NEW & NOTEWORTHY The present study uses self-referencing H+-selective electrodes for the first time to measure H+ fluxes from Müller (glial) cells isolated from tiger salamander retina. These studies demonstrate bicarbonate transport as a potent regulator of extracellular levels of acidity around Müller cells and point toward a need for further studies aimed at addressing how such glial cell pH regulatory mechanisms may shape neuronal signaling.

Pharmacological characterization of P2Y receptor subtypes on isolated tiger salamander Müller cells

Glia ◽  
2003 ◽  
Vol 42 (2) ◽  
pp. 149-159 ◽  
Author(s):  
Jenny M. Reifel Saltzberg ◽  
Katherine A. Garvey ◽  
Susan A. Keirstead
Keyword(s):  
Müller Cells ◽  
Receptor Subtypes ◽  
Tiger Salamander ◽  
P2y Receptor ◽  
Muller Cells ◽  
Pharmacological Characterization

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.

scholarly journals Melatonin attenuates oxidative stress and inflammation of Müller cells in diabetic retinopathy via activating the Sirt1 pathway

2021 ◽  
Vol 137 ◽  
pp. 111274
Author(s):  
Yuanyuan Tu ◽  
E Song ◽  
Zhenzhen Wang ◽  
Na Ji ◽  
Linling Zhu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Retinopathy ◽  
Müller Cells ◽  
Muller Cells

Vitreous from idiopathic epiretinal membrane patients induces glial-to-mesenchymal transition in Müller cells

2021 ◽  
pp. 166181
Author(s):  
Adwaid Manu Krishna Chandran ◽  
Daniela Coltrini ◽  
Mirella Belleri ◽  
Sara Rezzola ◽  
Elena Gambicorti ◽  
...  
Keyword(s):  
Epiretinal Membrane ◽  
Müller Cells ◽  
Muller Cells ◽  
Mesenchymal Transition ◽  
Idiopathic Epiretinal Membrane
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