Distribution of orthogonal arrays of particles in the Müller cell membrane of the mouse retina

Glia ◽  
1988 ◽  
Vol 1 (4) ◽  
pp. 246-252 ◽  
Author(s):  
Hartwig Wolburg ◽  
Karin Berg
Keyword(s):  
Cell Membrane ◽  
Orthogonal Arrays ◽  
Müller Cell ◽  
Mouse Retina ◽  
Orthogonal Arrays Of Particles ◽  
Muller Cell

scholarly journals Modulation of Muller cell membrane organization by 24S-hydroxycholesterol

2017 ◽  
Vol 95 ◽  
Author(s):  
P.H. Gabrielle ◽  
S. Gambert ◽  
E. Masson ◽  
E. Leger-Charnay ◽  
A. Ferrerro ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Müller Cell ◽  
Membrane Organization ◽  
Muller Cell

scholarly journals Targeted deletion of β1‐syntrophin causes a loss of K ir 4.1 from Müller cell endfeet in mouse retina

Glia ◽  
2019 ◽  
Vol 67 (6) ◽  
pp. 1138-1149 ◽  
Author(s):  
Shreyas B. Rao ◽  
Shirin Katoozi ◽  
Nadia Skauli ◽  
Stanley C. Froehner ◽  
Ole Petter Ottersen ◽  
...  
Keyword(s):  
Müller Cell ◽  
Mouse Retina ◽  
Targeted Deletion ◽  
Muller Cell

Cholesterol metabolism and glaucoma: Modulation of Muller cell membrane organization by 24S-hydroxycholesterol

2017 ◽  
Vol 207 ◽  
pp. 179-191 ◽  
Author(s):  
Ségolène Gambert ◽  
Pierre-Henry Gabrielle ◽  
Elodie Masson ◽  
Elise Leger-Charnay ◽  
Arthur Ferrerro ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Cholesterol Metabolism ◽  
Müller Cell ◽  
Membrane Organization ◽  
Muller Cell

Demonstration of Retinal Glycogen with Silver Methenamine

1971 ◽  
Vol 29 ◽  
pp. 564-565
Author(s):  
A. W. Sedar ◽  
G. H. Bresnick
Keyword(s):  
Lactic Acid ◽  
Chromic Acid ◽  
Periodic Acid ◽  
Müller Cell ◽  
External Limiting Membrane ◽  
Electron Microscope Level ◽  
Reactive Process ◽  
Inner Limiting Membrane ◽  
Muller Cell ◽  
And Migration

After experimetnal damage to the retina with a variety of procedures Müller cell hypertrophy and migration occurs. According to Kuwabara and others the reactive process in these injuries is evidenced by a marked increase in amount of glycogen in the Müller cells. These cells were considered originally supporting elements with fiber processes extending throughout the retina from inner limiting membrane to external limiting membrane, but are known now to have high lactic acid dehydrogenase activity and the ability to synthesize glycogen. Since the periodic acid-chromic acid-silver methenamine technique was shown to demonstrate glycogen at the electron microscope level, it was selected to react with glycogen in the fine processes of the Müller cell that ramify among the neural elements in various layers of the retina and demarcate these cells cytologically. The Rhesus monkey was chosen as an example of a well vascularized retina and the rabbit as an example of a avascular retina to explore the possibilities of the technique.

scholarly journals VEGF Mediates Retinal Müller Cell Viability and Neuroprotection through BDNF in Diabetes

Biomolecules ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 712
Author(s):  
Yun-Zheng Le ◽  
Bei Xu ◽  
Ana J. Chucair-Elliott ◽  
Huiru Zhang ◽  
Meili Zhu
Keyword(s):  
Specific Protein ◽  
Müller Cell ◽  
Dependent Manner ◽  
Vascular Abnormalities ◽  
Extracellular Signal ◽  
Muller Cell ◽  
Protein Kinase Akt ◽  
Sirna Knockdown ◽  
Endothelial Growth Factor ◽  
Dose Dependent

To investigate the mechanism of vascular endothelial growth factor (VEGF) and brain-derived neurotrophic factor (BDNF) in Müller cell (MC) viability and neuroprotection in diabetic retinopathy (DR), we examined the role of VEGF in MC viability and BDNF production, and the effect of BDNF on MC viability under diabetic conditions. Mouse primary MCs and cells of a rat MC line, rMC1, were used in investigating MC viability and BDNF production under diabetic conditions. VEGF-stimulated BDNF production was confirmed in mice. The mechanism of BDNF-mediated MC viability was examined using siRNA knockdown. Under diabetic conditions, recombinant VEGF (rVEGF) stimulated MC viability and BDNF production in a dose-dependent manner. rBDNF also supported MC viability in a dose-dependent manner. Targeting BDNF receptor tropomyosin receptor kinase B (TRK-B) with siRNA knockdown substantially downregulated the activated (phosphorylated) form of serine/threonine-specific protein kinase (AKT) and extracellular signal-regulated kinase (ERK), classical survival and proliferation mediators. Finally, the loss of MC viability in TrkB siRNA transfected cells under diabetic conditions was rescued by rBDNF. Our results provide direct evidence that VEGF is a positive regulator for BDNF production in diabetes for the first time. This information is essential for developing BDNF-mediated neuroprotection in DR and hypoxic retinal diseases, and for improving anti-VEGF treatment for these blood–retina barrier disorders, in which VEGF is a major therapeutic target for vascular abnormalities.

scholarly journals Involvement of NT3 and P75NTR in photoreceptor degeneration following selective Müller cell ablation

2013 ◽  
Vol 10 (1) ◽  
pp. 137 ◽  
Author(s):  
Weiyong Shen ◽  
Ling Zhu ◽  
So-Ra Lee ◽  
Sook H Chung ◽  
Mark C Gillies
Keyword(s):  
Müller Cell ◽  
Photoreceptor Degeneration ◽  
Cell Ablation ◽  
Muller Cell

Temporary impairment of Müller cell metabolism in the rat retina by intravitreal injection of fluorocitrate

1991 ◽  
Vol 53 (1) ◽  
pp. 115-122 ◽  
Author(s):  
M. Virgili ◽  
R. Paulsen ◽  
L. Villani ◽  
A. Contestabile ◽  
F. Fonnum
Keyword(s):  
Intravitreal Injection ◽  
Cell Metabolism ◽  
Müller Cell ◽  
Rat Retina ◽  
Muller Cell

scholarly journals Extracellular K+ activity changes related to electroretinogram components. I. Amphibian (I-type) retinas.

1985 ◽  
Vol 85 (6) ◽  
pp. 885-909 ◽  
Author(s):  
E Dick ◽  
R F Miller
Keyword(s):  
Profile Analysis ◽  
Müller Cell ◽  
Extracellular Potassium ◽  
Pharmacological Properties ◽  
Pharmacological Agents ◽  
Activity Measurements ◽  
Slow Piii ◽  
Muller Cell ◽  
Depolarizing Bipolar Cell ◽  
K Activity

Electroretinographic (ERG) and extracellular potassium activity measurements were carried out in superfused eyecup preparations of several amphibians. Light-evoked changes in extracellular K+ activity were characterized on the bases of depth profile analysis and latency measurements and through the application of pharmacological agents that have selective actions on the retinal network. Three different extracellular potassium modulations evoked at light onset were identified and characterized according to their phenomenological and pharmacological properties. These modulations include two separable sources of light-evoked increases in extracellular K+: (a) a proximal source that is largely post-bipolar in origin, and (b) a distal source that is primarily or exclusively of depolarizing bipolar cell origin. The pharmacological properties of the distal extracellular potassium increase closely parallel those of the b-wave. A distal light-evoked decrease in extracellular potassium appears to be associated with the slow PIII potential, based on a combination of simultaneous intracellular Müller cell recordings and extracellular ERG and potassium activity measurements before and during pharmacological isolation of the photoreceptor responses. The extracellular potassium activity increases are discussed with respect to the Müller cell theory of b-wave generation.

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