A quantitative study of the lateral spread of Müller cell responses to retinal lesions in the rabbit

1993 ◽  
Vol 334 (4) ◽  
pp. 545-558 ◽  
Author(s):  
M. F. Humphrey ◽  
I. J. Constable ◽  
Y. Chu ◽  
S. Wiffen
Keyword(s):  
Quantitative Study ◽  
Müller Cell ◽  
Lateral Spread ◽  
Retinal Lesions ◽  
Cell Responses ◽  
Muller Cell

PII component of the toad electroretinogram

1992 ◽  
Vol 68 (1) ◽  
pp. 333-341 ◽  
Author(s):  
B. J. Katz ◽  
Z. Xu ◽  
J. Zheng ◽  
B. Oakley
Keyword(s):  
Excitatory Amino Acid ◽  
Cell Activity ◽  
Plexiform Layer ◽  
Müller Cell ◽  
Light Responses ◽  
M Wave ◽  
Cell Responses ◽  
Ion Sensitive Microelectrodes ◽  
Muller Cell ◽  
Dc Component

1. The PII component of the electroretinogram (ERG) is comprised of the b-wave and the DC component and is thought to reflect bipolar cell activity. Although the b-wave is generated in large part by a K+/Muller cell mechanism, the origin of the DC component is unclear. In this paper we detail our investigation of the origin of the DC component. We hypothesize that the DC component is generated by a K+/Muller cell mechanism identical to that involved in b-wave generation. 2. We studied the ERG in the dark-adapted, isolated retina preparation of the toad, Bu fo marinus. We used K+ ion-sensitive microelectrodes (K+ISM), as well as conventional intra- and extracellular microelectrodes, to record [K+]o changes, the vitreal ERG, and Muller cell responses. 3. We used the excitatory amino acid receptor agonist N-methyl-DL-aspartate (NMDLA) to inhibit light responses of third-order neurons and thereby eliminate most of the ERG M-wave. In the absence of the M-wave, the ERG consisted of PII and PIII. We then superfused the retina with a solution containing both kynurenic acid (KYN) and 2-amino-4-phosphonobutyric acid (APB), which together inhibit all retinal responses proximal to the photoreceptors. In the presence of KYN and APB, the ERG consisted only of PIII. Using digital subtraction, we reconstructed PII. To our knowledge, this is the first report of the isolation of a PII component in the ERG of a nonmammalian species. 4. Using K+ISMs, we recorded the distal K+ changes in the outer plexiform layer (OPL).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Neurons, potassium, and glia in proximal retina of Necturus.

1980 ◽  
Vol 75 (2) ◽  
pp. 141-162 ◽  
Author(s):  
C J Karwoski ◽  
L M Proenza
Keyword(s):  
Time Course ◽  
Primary Source ◽  
Amacrine Cells ◽  
Müller Cell ◽  
Wave Form ◽  
Cell Responses ◽  
Decay Times ◽  
Low Pass ◽  
Muller Cell ◽  
Time Courses

Light-evoked K+ flux and intracellular Müller (glial) cell and on/off-neuron responses were recorded from the proximal retina of Necturus in eyecups from which the vitreous was not drained. On/off-responses, probably arising from amacrine cells, showed an initial transient and a sustained component that always exhibited surround antagonism. Müller cell responses were small but otherwise similar to those recorded in eyecups drained of vitreous. The proximal K+ increase and Müller cell responses had identical decay times, and on some occasions the latency and rise time of the K+ increase nearly matched Müller cell responses, indicating that the recorded K+ responses were not always appreciably degraded by electrode "dead space." The spatiotemporal distribution of the K+ increase showed that both diffusion and active reuptake play important roles in K+ clearance. The relationship between on/off-neuron responses and the K+ increase was modelled by assuming that (a) K+ release is positively related to the instantaneous amplitude of the neural response, and (b) K+ accumulating in extracellular space is cleared via mechanisms with approximately exponential time-courses. These two processes were approximated by low-pass filtering the on/off-neuron responses, resulting in modelled responses that match the wave form and time-course of the K+ increase and behave quantitatively like the K+ increase to changes in stimulus intensity and diameter. Thus, on/off-neurons are probably a primary source of the proximal light-evoked K+ increase that depolarizes glial cells to generate the M-wave.

scholarly journals Adaptive Müller cell responses to microglial activation mediate neuroprotection and coordinate inflammation in the retina

2011 ◽  
Vol 8 (1) ◽  
pp. 173 ◽  
Author(s):  
Minhua Wang ◽  
Wenxin Ma ◽  
Lian Zhao ◽  
Robert N Fariss ◽  
Wai T Wong
Keyword(s):  
Microglial Activation ◽  
Müller Cell ◽  
Cell Responses ◽  
Muller Cell

First Responders: Dynamics of Pre-Gliotic Müller Cell Responses in The Isolated Adult Rat Retina

2014 ◽  
Vol 40 (12) ◽  
pp. 1245-1260 ◽  
Author(s):  
Linnéa Taylor ◽  
Karin Arnér ◽  
Fredrik Ghosh
Keyword(s):  
First Responders ◽  
Müller Cell ◽  
Rat Retina ◽  
Adult Rat ◽  
Cell Responses ◽  
Muller Cell

Relationship between Muller cell responses, a local transretinal potential, and potassium flux

1977 ◽  
Vol 40 (2) ◽  
pp. 244-259 ◽  
Author(s):  
C. J. Karowski ◽  
L. M. Proenza
Keyword(s):  
Müller Cells ◽  
Müller Cell ◽  
Extracellular Potassium ◽  
Muller Cells ◽  
Light Onset ◽  
M Wave ◽  
Cell Responses ◽  
Stimulus Parameters ◽  
Muller Cell ◽  
Cell Depolarization

1. In the Necturus retina, light-evoked field potentials, Muller (glial) cell responses, and extracellular potassium ion concentration ([K+]0) were recorded and found to exhibit the three-way correlation characteristic of these variables elsewhere in the nervous system. 2. Muller cell responses to a flashed spot or annulus consist primarily of slow depolarizations at both light onset and offset. The responses are maximum to 0.5-mm-diameter spots and decrease with larger diameters. Responses to stimulus intensity and flicker were also used to characterize Muller cell behavior. 3. In response to long-duration stimuli, the initial Muller cell depolarization is followed by a very slow hyperpolarization, which is likely the origin of slow PIII. 4. A new extracellular potential is described, the M-wave, the basic properties of which suggest that it is generated by Muller cells. Moreover, the M-wave and Muller cells show remarkably similar behavior to a wide variety of stimulus parameters. 5. In the proximal retina, [K+]0 increases at both light onset and offset with a time course similar to that of Muller cell depolarizing responses. This K+ increase also behaves similarly to the Muller cell depolarization in response to changes in stimulus parameters. 6. It is concluded that light stimulation leads to an increase in [K+]0 in the proximal retina and that this increase depolarizes Muller cells whose associated currents, in turn, generate the M-wave.

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
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