Bibliografie tematiche / Retinal ganglion cells

Letteratura scientifica selezionata sul tema "Retinal ganglion cells"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 9 marzo 2023

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Articoli di riviste sul tema "Retinal ganglion cells"

1

Reinhard, Katja, e Thomas A. Münch. "Visual properties of human retinal ganglion cells". PLOS ONE 16, n. 2 (16 febbraio 2021): e0246952. http://dx.doi.org/10.1371/journal.pone.0246952.

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Abstract (sommario):
The retinal output is the sole source of visual information for the brain. Studies in non-primate mammals estimate that this information is carried by several dozens of retinal ganglion cell types, each informing the brain about different aspects of a visual scene. Even though morphological studies of primate retina suggest a similar diversity of ganglion cell types, research has focused on the function of only a few cell types. In human retina, recordings from individual cells are anecdotal or focus on a small subset of identified types. Here, we present the first systematic ex-vivo recording of light responses from 342 ganglion cells in human retinas obtained from donors. We find a great variety in the human retinal output in terms of preferences for positive or negative contrast, spatio-temporal frequency encoding, contrast sensitivity, and speed tuning. Some human ganglion cells showed similar response behavior as known cell types in other primate retinas, while we also recorded light responses that have not been described previously. This first extensive description of the human retinal output should facilitate interpretation of primate data and comparison to other mammalian species, and it lays the basis for the use of ex-vivo human retina for in-vitro analysis of novel treatment approaches.
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2

Kanamoto, Takashi, Yasushi Kitaoka, Hiroaki Sakaue, Yusuke Murakami, Yasuhiro Ikeda, Kei Tobiume e Yoshiaki Kiuchi. "D-Serine Induced by Ocular Hypertension is Associated with Retinal Cell Death". Current Trends in Ophthalmology 1, n. 1 (3 luglio 2018): 23–29. http://dx.doi.org/10.18314/ctoy.v1i1.1161.

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Abstract (sommario):
Purpose: The purpose of this study is to investigate the role of free D-serine in the death of retinal cells caused by ocular hypertension.Methods: Adult Wistar rats were used as an experimental model of ocular hypertension. Immunohistochemistry was used to identify the retinal sites and expression patterns of D-serine and serine racemase in the rat retina. The concentrations of free D-serine and L-serine in the retina were measured by two-dimensional high-performance liquid chromatography. Retinal cell death was investigated by Immunohistochemistry.Results: D-serine was expressed on the retinal ganglion cell layer in the retinas of rats with ocular hypertension. A serine racemase was specifically expressed in the retinal ganglion cells. The ratio of free D-/L-serine in the retinas with ocular hypertension was higher than that in the retinas with normal tension. Annexing-V-positive cells were observed in the retinal ganglion cell layer in the retinas of the rats with ocular hypertension, and these cells were also co-localized with D-serine expression.Conclusions: We suspect that the up-regulation of serine racemase expression induced by ocular hypertensionleads to an increase in free D-serine converted from free L-serine in retinal ganglion cells and that retinal cell death is associated with D-serine expression.
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3

Wang, Steven W., Xiuqian Mu, William J. Bowers, Dong-Seob Kim, Daniel J. Plas, Michael C. Crair, Howard J. Federoff, Lin Gan e William H. Klein. "Brn3b/Brn3c double knockout mice reveal an unsuspected role for Brn3c in retinal ganglion cell axon outgrowth". Development 129, n. 2 (15 gennaio 2002): 467–77. http://dx.doi.org/10.1242/dev.129.2.467.

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Abstract (sommario):
In mice, Brn3 POU domain transcription factors play essential roles in the differentiation and survival of projection neurons within the retina, inner ear, dorsal root and trigeminal ganglia. During retinal ganglion cell differentiation, Brn3b is expressed first, followed by Brn3a and Brn3c. Targeted deletion of Brn3b, but not Brn3a or Brn3c, leads to a loss of most retinal ganglion cells before birth. However, as a few retinal ganglion cells are still present in Brn3b–/– mice, Brn3a and Brn3c may partially compensate for the loss of Brn3b. To examine the role of Brn3c in retinal ganglion cell development, we generated Brn3b/Brn3c double knockout mice and analyzed their retinas and optic chiasms. Retinal ganglion cell axons from double knockout mice were more severely affected than were those from Brn3b-deficient mice, indicating that Brn3c was required for retinal ganglion cell differentiation and could partially compensate for the loss of Brn3b. Moreover, Brn3c had functions in retinal ganglion cell differentiation separate from those of Brn3b. Ipsilateral and misrouted projections at the optic chiasm were overproduced in Brn3b–/– mice but missing were entirely in optic chiasms of Brn3b/Brn3c double knockout mice, suggesting that Brn3c controlled ipsilateral axon production. Forced expression of Brn3c in Brn3b–/– retinal explants restored neurite outgrowth, demonstrating that Brn3c could promote axon outgrowth in the absence of Brn3b. Our results reveal a complex genetic relationship between Brn3b and Brn3c in regulating the retinal ganglion cell axon outgrowth.
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Waid, D. K., e S. C. McLoon. "Ganglion cells influence the fate of dividing retinal cells in culture". Development 125, n. 6 (15 marzo 1998): 1059–66. http://dx.doi.org/10.1242/dev.125.6.1059.

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Abstract (sommario):
The different retinal cell types arise during vertebrate development from a common pool of progenitor cells. The mechanisms responsible for determining the fate of individual retinal cells are, as yet, poorly understood. Ganglion cells are one of the first cell types to be produced in the developing vertebrate retina and few ganglion cells are produced late in development. It is possible that, as the retina matures, the cellular environment changes such that it is not conducive to ganglion cell determination. The present study showed that older retinal cells secrete a factor that inhibits the production of ganglion cells. This was shown by culturing younger retinal cells, the test population, adjacent to various ages of older retinal cells. Increasingly older retinal cells, up to embryonic day 9, were more effective at inhibiting production of ganglion cells in the test cell population. Ganglion cell production was restored when ganglion cells were depleted from the older cell population. This suggests that ganglion cells secrete a factor that actively prevents cells from choosing the ganglion cell fate. This factor appeared to be active in medium conditioned by older retinal cells. Analysis of the conditioned medium established that the factor was heat stable and was present in the <3 kDa and >10 kDa fractions. Previous work showed that the neurogenic protein, Notch, might also be active in blocking production of ganglion cells. The present study showed that decreasing Notch expression with an antisense oligonucleotide increased the number of ganglion cells produced in a population of young retinal cells. Ganglion cell production, however, was still inhibited in cultures using antisense oligonucleotide to Notch in medium conditioned by older retinal cells. This suggests that the factor secreted by older retinal cells inhibits ganglion cell production through a different pathway than that mediated by Notch.
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Silveira, L. C. L., C. W. Picanço-Diniz e E. Oswaldo-Cruz. "Distribution and size of ganglion cells in the retinae of large Amazon rodents". Visual Neuroscience 2, n. 3 (marzo 1989): 221–35. http://dx.doi.org/10.1017/s0952523800001140.

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AbstractThe topographical distribution of density and soma size of the retinal ganglion cells were studied in three species of hystricomorph rodents. Flat-mounted retinae were stained by the Nissl method and the ganglion cells counted on a matrix covering the whole retinae. Soma size was determined for samples at different retinal regions. The agouti, a diurnal rodent, shows a well-developed visual streak, reaching a peak density of 6250 ganglion cells/mm2. The total number of ganglion cells ranged from 477, 427–548, 205 in eight retinae. The ganglion-cell-size histogram of the visual streak region exhibits a marked shift towards smaller values when compared to retinal periphery. Upper and lower regions differ in both cell density and cell size. The crepuscular capybara shows a less-developed visual streak with a peak ganglion cell density of 2250/mm2. The shift towards small-sized cells in the visual streak is less marked. Total ganglion cell population is 368,840. In the nocturnal paca, the upper half of the fundus oculi includes a tapetum lucidum. The retina of this species shows the least-developed visual streak of this group, with the lowest peak ganglion cell density reaching 925/mm2. The total ganglion cell number (230,804) is also smaller than in the two other species. Soma-size spectra of this species are characterized by the presence, in the lower hemi-retina, of very large perikarya comparable in size to the cat's alpha ganglion cells.
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6

Sekirnjak, Chris, Clare Hulse, Lauren H. Jepson, Pawel Hottowy, Alexander Sher, Wladyslaw Dabrowski, A. M. Litke e E. J. Chichilnisky. "Loss of Responses to Visual But Not Electrical Stimulation in Ganglion Cells of Rats With Severe Photoreceptor Degeneration". Journal of Neurophysiology 102, n. 6 (dicembre 2009): 3260–69. http://dx.doi.org/10.1152/jn.00663.2009.

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Abstract (sommario):
Retinal implants are intended to help patients with degenerative conditions by electrically stimulating surviving cells to produce artificial vision. However, little is known about how individual retinal ganglion cells respond to direct electrical stimulation in degenerating retina. Here we used a transgenic rat model to characterize ganglion cell responses to light and electrical stimulation during photoreceptor degeneration. Retinas from pigmented P23H-1 rats were compared with wild-type retinas between ages P37 and P752. During degeneration, retinal thickness declined by 50%, largely as a consequence of photoreceptor loss. Spontaneous electrical activity in retinal ganglion cells initially increased two- to threefold, but returned to nearly normal levels around P600. A profound decrease in the number of light-responsive ganglion cells was observed during degeneration, culminating in retinas without detectable light responses by P550. Ganglion cells from transgenic and wild-type animals were targeted for focal electrical stimulation using multielectrode arrays with electrode diameters of ∼10 microns. Ganglion cells were stimulated directly and the success rate of stimulation in both groups was 60–70% at all ages. Surprisingly, thresholds (∼0.05 mC/cm2) and latencies (∼0.25 ms) in P23H rat ganglion cells were comparable to those in wild-type ganglion cells at all ages and showed no change over time. Thus ganglion cells in P23H rats respond normally to direct electrical stimulation despite severe photoreceptor degeneration and complete loss of light responses. These findings suggest that high-resolution epiretinal prosthetic devices may be effective in treating vision loss resulting from photoreceptor degeneration.
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Troilo, David, Meijuan Xiong, Justin C. Crowley e Barbara L. Finlay. "Factors controlling the dendritic arborization of retinal ganglion cells". Visual Neuroscience 13, n. 4 (luglio 1996): 721–33. http://dx.doi.org/10.1017/s0952523800008609.

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AbstractThe effects of changing retinal ganglion cell (RGC) density and availability of presynaptic sites on the development of RGC dendritic arbor in the developing chick retina were contrasted. Visual form deprivation was used to induce ocular enlargement and expanded retinal area resulting in a 20–30% decrease in RGC density. In these retinas, RGC dendritic arbors increased in a compensatory manner to maintain the inner nuclear layer to RGC convergence ratio in a way that is consistent with simple stretching; RGC dendritic arbors become larger with increased branch lengths, but without change in the total number of branches. In the second manipulation, partial optic nerve section was used to produce areas of RGC depletion of approximately 60% in the central retina. This reduction in density is comparable to the density of locations in the normal peripheral retina. In RGC-depleted retinas, dendritic arbor areas of RGCs in the central retina grow to match the size of normal peripheral arbors. In contrast to the expanded case, two measures of intrinsic arbor structure are changed in RGC-depleted retinas; the branch density of RGC dendrites is greater, and the relative areas of the two arbors of bistratified cells are altered. We discuss the potential roles of retinal growth, local RGC density, and availability of presynaptic terminals in the developmental control of RGC dendritic arbor.
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Grosberg, Lauren E., Karthik Ganesan, Georges A. Goetz, Sasidhar S. Madugula, Nandita Bhaskhar, Victoria Fan, Peter Li et al. "Activation of ganglion cells and axon bundles using epiretinal electrical stimulation". Journal of Neurophysiology 118, n. 3 (1 settembre 2017): 1457–71. http://dx.doi.org/10.1152/jn.00750.2016.

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Abstract (sommario):
Epiretinal prostheses for treating blindness activate axon bundles, causing large, arc-shaped visual percepts that limit the quality of artificial vision. Improving the function of epiretinal prostheses therefore requires understanding and avoiding axon bundle activation. This study introduces a method to detect axon bundle activation on the basis of its electrical signature and uses the method to test whether epiretinal stimulation can directly elicit spikes in individual retinal ganglion cells without activating nearby axon bundles. Combined electrical stimulation and recording from isolated primate retina were performed using a custom multielectrode system (512 electrodes, 10-μm diameter, 60-μm pitch). Axon bundle signals were identified by their bidirectional propagation, speed, and increasing amplitude as a function of stimulation current. The threshold for bundle activation varied across electrodes and retinas, and was in the same range as the threshold for activating retinal ganglion cells near their somas. In the peripheral retina, 45% of electrodes that activated individual ganglion cells (17% of all electrodes) did so without activating bundles. This permitted selective activation of 21% of recorded ganglion cells (7% of expected ganglion cells) over the array. In one recording in the central retina, 75% of electrodes that activated individual ganglion cells (16% of all electrodes) did so without activating bundles. The ability to selectively activate a subset of retinal ganglion cells without axon bundles suggests a possible novel architecture for future epiretinal prostheses. NEW & NOTEWORTHY Large-scale multielectrode recording and stimulation were used to test how selectively retinal ganglion cells can be electrically activated without activating axon bundles. A novel method was developed to identify axon activation on the basis of its unique electrical signature and was used to find that a subset of ganglion cells can be activated at single-cell, single-spike resolution without producing bundle activity in peripheral and central retina. These findings have implications for the development of advanced retinal prostheses.
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Greco, Jordan A., Nicole L. Wagner, Ralph J. Jensen, Daniel B. Lawrence, Matthew J. Ranaghan, Megan N. Sandberg, Daniel J. Sandberg e Robert R. Birge. "Activation of retinal ganglion cells using a biomimetic artificial retina". Journal of Neural Engineering 18, n. 6 (1 dicembre 2021): 066027. http://dx.doi.org/10.1088/1741-2552/ac395c.

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Abstract (sommario):
Abstract Objective. Biomimetic protein-based artificial retinas offer a new paradigm for restoring vision for patients blinded by retinal degeneration. Artificial retinas, comprised of an ion-permeable membrane and alternating layers of bacteriorhodopsin (BR) and a polycation binder, are assembled using layer-by-layer electrostatic adsorption. Upon light absorption, the oriented BR layers generate a unidirectional proton gradient. The main objective of this investigation is to demonstrate the ability of the ion-mediated subretinal artificial retina to activate retinal ganglion cells (RGCs) of degenerated retinal tissue. Approach. Ex vivo extracellular recording experiments with P23H line 1 rats are used to measure the response of RGCs following selective stimulation of our artificial retina using a pulsed light source. Single-unit recording is used to evaluate the efficiency and latency of activation, while a multielectrode array (MEA) is used to assess the spatial sensitivity of the artificial retina films. Main results. The activation efficiency of the artificial retina increases with increased incident light intensity and demonstrates an activation latency of ∼150 ms. The results suggest that the implant is most efficient with 200 BR layers and can stimulate the retina using light intensities comparable to indoor ambient light. Results from using an MEA show that activation is limited to the targeted receptive field. Significance. The results of this study establish potential effectiveness of using an ion-mediated artificial retina to restore vision for those with degenerative retinal diseases, including retinitis pigmentosa.
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Vlasiuk, Anastasiia, e Hiroki Asari. "Feedback from retinal ganglion cells to the inner retina". PLOS ONE 16, n. 7 (22 luglio 2021): e0254611. http://dx.doi.org/10.1371/journal.pone.0254611.

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Abstract (sommario):
Retinal ganglion cells (RGCs) are thought to be strictly postsynaptic within the retina. They carry visual signals from the eye to the brain, but do not make chemical synapses onto other retinal neurons. Nevertheless, they form gap junctions with other RGCs and amacrine cells, providing possibilities for RGC signals to feed back into the inner retina. Here we identified such feedback circuitry in the salamander and mouse retinas. First, using biologically inspired circuit models, we found mutual inhibition among RGCs of the same type. We then experimentally determined that this effect is mediated by gap junctions with amacrine cells. Finally, we found that this negative feedback lowers RGC visual response gain without affecting feature selectivity. The principal neurons of the retina therefore participate in a recurrent circuit much as those in other brain areas, not being a mere collector of retinal signals, but are actively involved in visual computations.
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Tesi sul tema "Retinal ganglion cells"

1

Grumet, Andrew Eli. "Extracellular electrical stimulation of retinal ganglion cells". Thesis, Massachusetts Institute of Technology, 1994. http://hdl.handle.net/1721.1/42559.

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Davenport, Christopher M. "Neural circuitry of retinal receptive fields in primate /". Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/10652.

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Uzzell, Valerie Joy. "Sensitivity and noise in primate retinal ganglion cells /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2005. http://wwwlib.umi.com/cr/ucsd/fullcit?p3190165.

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Fok, Lai-chun. "Neuroprotection of retinal ganglion cells with laser therapy". Click to view the E-thesis via HKUTO, 1999. http://sunzi.lib.hku.hk/hkuto/record/B31969616.

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Fok, Lai-chun, e 霍麗珍. "Neuroprotection of retinal ganglion cells with laser therapy". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31969616.

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Mellough, Carla Bernadette. "An assessment of the cell replacement capability of immortalised, clonal and primary neural tissues following their intravitreal transplantation into rodent models of selective retinal ganglion cell depletion". University of Western Australia. School of Anatomy and Human Biology, 2005. http://theses.library.uwa.edu.au/adt-WU2005.0101.

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[Truncated abstract] Microenvironmental changes associated with apoptotic neural degeneration may instruct a proportion of newly transplanted donor cells to differentiate towards the fate of the deteriorating host cellular phenotype. In the work described in this thesis, this hypothesis was tested by inducing apoptotic retinal ganglion cell (RGC) death in neonatal and adult rats and mice, and then examining whether intravitreally grafted cells from a range of sources of donor neural tissue became incorporated into these selectively depleted retinae. Donor tissues were: a postnatal murine cerebellar-derived immortalised neural precursor cell line (C17.2); an adult rat hippocampal-derived clonal stem-like line (HCN/GFP); mouse embryonic day 14 (E14) primary dissociated retinal cells (Gt[ROSA]26); and adult mouse ciliary pigmented margin-derived primary neurospheres (Gt[ROSA]26). In neonates, rapid RGC death was induced by removal of the contralateral superior colliculus (SC), and in adults, delayed RGC death was induced by unilateral optic nerve (ON) transection. Some adult hosts received ON transection coupled with an autologous peripheral nerve (PN) graft. Donor cells were injected intravitreally 6-48 h after SC ablation (neonates) or 0, 5, 7 or 14 days after ON injury (adults). Cells were also injected into non-RGC depleted neonatal and adult retinae. At 4 or 8 weeks, transplanted cells were identified, quantified and their differentiation fate within host retinae was assessed. Transplanted male C17.2 cells were identified in host retinae using a Y-chromosome marker and in situ hybridisation, or by their expression of the lacZ reporter gene product Escherichia coli beta-galactosidase (beta-gal) using Xgal histochemistry or a beta-gal antibody. No C17.2 cells were identified in axotomised adult-injected eyes undergoing delayed RGC apoptosis (n = 16). Donor cells were, however, stably integrated within the retina in 29% (15/55) of mice that received C17.2 cell injections 24 h after neonatal SC ablation; 6-31% of surviving cells were found in the RGC layer (GCL). These NSC-like cells were also present in intact retinae, but on average there were fewer cells in GCL. In SC-ablated mice, most grafted cells did not express retinal-specific markers, although occasional donor cells in the GCL were immunopositive for beta-III tubulin (TUJ1), a protein highly iii expressed by, but not specific to, developing RGCs. Targeted rapid RGC depletion thus increased C17.2 cell incorporation into the GCL, but grafted C17.2 cells did not appear to differentiate into an RGC phenotype.
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Li, Suk-yee. "Functional changes and differential cell death of retinal ganglion cells after injury". View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B37552612.

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Li, Suk-yee, e 李淑儀. "Functional changes and differential cell death of retinal ganglion cells after injury". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B38597731.

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Lau, Hoi-shan Flora. "Retinal ganglion cells vulnerability in a rat glaucoma model /". View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31495217.

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Lau, Hoi-shan Flora, e 劉凱珊. "Retinal ganglion cells vulnerability in a rat glaucoma model". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45010250.

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Libri sul tema "Retinal ganglion cells"

1

Neuronal Diversification Within the Retina: Generation of Crossed and Uncrossed Retinal Ganglion Cells. [New York, N.Y.?]: [publisher not identified], 2013.

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2

M, Shapley R., e Lam Dominic Man-Kit, a cura di. Contrast sensitivity. Cambridge, Mass: MIT Press, 1993.

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Moore, Matthew R. Central nervous system regeneration: Survival of retinal ganglion cells and optic nerve in mouse following axotomy and grafting. [New Haven: s.n.], 1986.

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Raza, Ali Syed. Modeling the Structure-Function Relationship between Retinal Ganglion Cells and Visual Field Sensitivity and the Changes Due to Glaucomatous Neuropathy. [New York, N.Y.?]: [publisher not identified], 2014.

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Rajaraman, Kaveri. Intrinsically photosensitive ganglion cells of the tiger salamander retina. Cambridge, Mass: Harvard University, 2009.

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Vlastimil, Liora G. Ganglion Cells: Morphology, Functional Development and Role in Disease. Nova Science Publishers, Incorporated, 2014.

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Yang, Jing. Updates on Intrinsically Photosensitive Retinal Ganglion Cells. Scientific Research Publishing, 2021.

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Hong, Youn-Young Kate. Structure and development of retinal ganglion cells. 2010.

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Yang, Jing. Updates on Intrinsically Photosensitive Retinal Ganglion Cells. Scientific Research Publishing, 2021.

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Joyce, Daniel S., Kevin W. Houser, Stuart N. Peirson, Jamie M. Zeitzer e Andrew J. Zele. Melanopsin Vision: Sensation and Perception Through Intrinsically Photosensitive Retinal Ganglion Cells. Cambridge University Press, 2023.

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Capitoli di libri sul tema "Retinal ganglion cells"

1

Dubin, Mark Wm. "Retinal Ganglion Cells". In Sensory System I, 53–54. Boston, MA: Birkhäuser Boston, 1988. http://dx.doi.org/10.1007/978-1-4899-6647-6_26.

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Lucas, Robert. "Melanopsin Retinal Ganglion Cells". In Encyclopedia of Color Science and Technology, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27851-8_275-1.

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Lucas, Robert. "Melanopsin Retinal Ganglion Cells". In Encyclopedia of Color Science and Technology, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-642-27851-8_275-2.

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Lucas, Robert. "Melanopsin Retinal Ganglion Cells". In Encyclopedia of Color Science and Technology, 901–3. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4419-8071-7_275.

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Lupinacci, Alvaro P. C., Howard Barnebey e Peter A. Netland. "Neuroprotection of Retinal Ganglion Cells". In The Glaucoma Book, 647–50. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-0-387-76700-0_54.

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Pickard, Gary E., e Patricia J. Sollars. "Intrinsically Photosensitive Retinal Ganglion Cells". In Reviews of Physiology, Biochemistry and Pharmacology 162, 59–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/112_2011_4.

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Križaj, David. "Polymodal Sensory Integration in Retinal Ganglion Cells". In Retinal Degenerative Diseases, 693–98. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17121-0_92.

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Sluch, Valentin M., e Donald J. Zack. "Stem Cells, Retinal Ganglion Cells and Glaucoma". In Developments in Ophthalmology, 111–21. Basel: S. KARGER AG, 2014. http://dx.doi.org/10.1159/000358409.

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Santina, Luca Della, e Yvonne Ou. "Biolistic Labeling of Retinal Ganglion Cells". In Glaucoma, 161–70. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7407-8_14.

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Guo, Tianruo, David Tsai, Siwei Bai, Mohit Shivdasani, Madhuvanthi Muralidharan, Liming Li, Socrates Dokos e Nigel H. Lovell. "Insights from Computational Modelling: Selective Stimulation of Retinal Ganglion Cells". In Brain and Human Body Modeling 2020, 233–47. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-45623-8_13.

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AbstractImprovements to the efficacy of retinal neuroprostheses can be achieved by developing more sophisticated neural stimulation strategies to enable selective or differential activation of specific retinal ganglion cells (RGCs). Recent retinal studies have demonstrated the ability to differentially recruit ON and OFF RGCs – the two major information pathways of the retina – using high-frequency electrical stimulation (HFS). However, there remain many unknowns, since this is a relatively unexplored field. For example, can we achieve ON/OFF selectivity over a wide range of stimulus frequencies and amplitudes? Furthermore, existing demonstrations of HFS efficacy in retinal prostheses have been based on epiretinal placement of electrodes. Other clinically popular techniques include subretinal or suprachoroidal placement, where electrodes are located at the photoreceptor layer or in the suprachoroidal space, respectively, and these locations are quite distant from the RGC layer. Would HFS-based differential activation work from these locations? In this chapter, we conducted in silico investigations to explore the generalizability of HFS to differentially active ON and OFF RGCs. Computational models are particularly well suited for these investigations. The electric field can be accurately described by mathematical formulations, and simulated neurons can be “probed” at resolutions well beyond those achievable by today’s state-of-the-art experimental techniques.
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Atti di convegni sul tema "Retinal ganglion cells"

1

Lennie, Peter. "Retinal receptive fields and eccentricity". In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1985. http://dx.doi.org/10.1364/oam.1985.thf1.

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In animals like cat and monkey, which have a specialized central area in the retina, the distribution of photoreceptors and the organization of their connections to the brain change greatly as one moves from the central to the peripheral retina. This is reflected in several properties of retinal ganglion cells whose axons form the optic nerve. The density of cells is highest in the central area and, despite the fact that the smallest receptive fields are found there, the overlap of receptive fields is generally greatest. Increasing eccentricity leads to reduced density of cells, larger receptive fields, and some changes in the temporal characteristics of their responses. The interpretation of these observations is made more complicated by the fact that in both species several distinct classes of ganglion cell have been identified and these differ in their distributions on the retina. The purpose of the talk is to characterize the general changes in properties of retinal ganglion cells that occur as one moves from the central to the peripheral retina and to compare the representations of the image transmitted by the different classes of cell.
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2

Heussner, N., S. Schnichels, M. Spitzer, K. U. Bartz-Schmidt e W. Stork. "Laser excitation of retinal ganglion cells". In 2011 10th International Workshop on Biomedical Engineering. IEEE, 2011. http://dx.doi.org/10.1109/iwbe.2011.6079042.

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3

Raninen, Antti, Rauli Franssila e Jyrki Rovamo. "Critical flicker frequency as a function of photopic luminous flux across the human visual field". In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1989. http://dx.doi.org/10.1364/oam.1989.wm4.

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Using the method of adjustment and a panel of 256 LEDs (dominant wavelength 640 nm) mounted in a solid, black enclosure and covered with a white diffusion screen, we measured CFF to cone stimuli (sinusoidal luminance modulation of 30%) across the temporal visual field at three different levels of retinal illuminance (1970,123, and 25.0 phot, td) produced by inserting neutral density filters (Lee) in front of the panel. Retinal illuminance was constant at all eccentricities studied because retinal area per one solid degree of visual field and effective pupillary area decrease similarly when eccentricity increases from 0° to 80°. The stimuli were M-scaled1 to keep the number of ganglion cells stimulated at various eccentricities approximately constant (4400 cells). M-scaling was obtained by reducing the viewing distance in inverse proportion to the sampling density of ganglion cell receptive fields across the retina. CFF was found to increase monotonically with eccentricity but the increase was the steeper the higher the level of retinal illuminance, in agreement with our previous results.2 However, when plotted in double logarithmic coordinates, CFF was found to increase as a single linear function of photopic luminous flux (F) collected by retinal ganglion cells: CFF = 18 × F0.22 (r2 = 0.945). Flux was calculated by multiplying retinal illuminance with Ricco's area that provides an estimate for the average area of the human ganglion cell receptive field center at various retinal locations.
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4

Buchsbaum, G., e D. J. Miller. "Nonuniform subband coding by retinal ganglion cells". In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1990. http://dx.doi.org/10.1364/oam.1990.mt6.

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The lateral geniculate nucleus (LGN) in primates comprises cells with greatly varying numbers and contrast sensitivities. Cells in the magnocellular layers are approximately eight times more sensitive to luminance contrast than are the color-sensitive cells in the parvicellular layers. Parvicellular cells, on the other hand, outnumber magnocellular cells by approximately a factor of 10.1,2 Kaplan and Shapley1 report that these differences in contrast sensitivity result from differences in the sensitivity of the retinal ganglion cells that provide excitatory synaptic impulses to the LGN neurons. These cells, with varying sensitivities and densities, constitute an imagecoding scheme in which dense high-rate samples of an image with relatively low contrast sensitivity are supplemented with lower-density samples with better contrast sensitivity. If the few higher-contrast samples are sufficient to compensate for the low contrast of the densely populated cells when coding the image, then considerable dynamic contrast range can be saved.
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5

Muralidharan, Madhuvanthi, Tianruo Guo, Mohit N. Shivdasani, David Tsai, Shelley Fried, Morven Cameron, John W. Morley, Socrates Dokos e Nigel H. Lovell. "Towards Controlling Functionally-Distinct Retinal Ganglion Cells In Degenerate Retina". In 2020 42nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC) in conjunction with the 43rd Annual Conference of the Canadian Medical and Biological Engineering Society. IEEE, 2020. http://dx.doi.org/10.1109/embc44109.2020.9176595.

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6

Xiao, Lei, Ying-Ying Zhang e Pei-Ji Liang. "Dynamic Concerted Activities among Retinal Ganglion Cells". In 2010 4th International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2010. http://dx.doi.org/10.1109/icbbe.2010.5515002.

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7

Farah, Nairouz, Inna Reutsky e Shy Shoham. "Patterned Optical Activation of Retinal Ganglion Cells". In 2007 29th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2007. http://dx.doi.org/10.1109/iembs.2007.4353812.

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8

James, AC, T. Maddess, K. Rouhan, S. Bedford e M. Snowball. "Evidence for My-cell Involvement in the Spatial Frequency Doubled Illusion as Revealed by a Multiple Region PERG for Glaucoma". In Vision Science and its Applications. Washington, D.C.: Optica Publishing Group, 1995. http://dx.doi.org/10.1364/vsia.1995.tub3.

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Recent evidence suggests that glaucoma leads to early loss of large retinal ganglion cells1,2 projecting to the Magnocellular layers of the dLGN: the so called "M" retinal ganglion cells. It is necessary for the present study, to appreciate that there are two subgroups of M-cells, the Mx-cells which are quite linear, and the nonlinearly responding My-cells, where the subscripts indicate physiological similarities with cat X and Y-cells3. In particular the retinal gain control described by Shapley and Victor4 for cat X and Y cells is strongly expressed in primate M- cells5. Except at very low temporal frequencies the quadratic response of Y-cells is larger than the linear response, especially at low spatial frequencies6, and the gain control effects Y-cells more, especially their quadratic response7. At least three studies indicate that My-cells are larger than Mx- cells8,9,10. Therefore, methods for glaucoma diagnosis should perhaps appeal to My-cell physiology, e.g. the strong effects of gain control upon their nonlinear responses.
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9

Smith, Vivianne C., Joel Pokorny, Barry B. Lee, Paul R. Martin e Arne Valberg. "Cone inputs to macaque M-pathway (phasic) retinal ganglion cells". In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1989. http://dx.doi.org/10.1364/oam.1989.thv6.

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At ARVO 1989 we presented amplitude and phase data for macaque retinal ganglion cells to a temporal stimulus. Our stimulus presented 2000-td equiluminant red and green LEDs in temporal sine wave modulation. We measured ganglion cell responses as a function of physical phase difference between the LEDs. P-pathway (tonic) cells could be described by a linear model of the LWS and MWS cone inputs. M-pathway (phasic) cell behavior was more complicated. Phasic ON- and OFF-center cells showed similar amplitude behavior as a function of physical phase angle that paralleled psychophysical data for the same stimulus. The data suggested evidence of compound center-surround inputs: centers show (LWS + MWS) cone summation while surrounds show cone opponency and can be Red-On or Green-On. The phasic cells showed differing phase patterns. Some phasic cells showed a phase response dominated by L cones while others showed evidence of a phasic response dominated by M cones, giving four different phase patterns: ON-center with LWS cone phase, OFF-center with MWS cone phase, ON-center with MWS cone phase and OFF-center with LWS cone phase. The first two could be fit by an (LWS + MWS) center with an opponent surround that showed a fixed 90° phase shift, predicted by the quadrature nature of the stimulus. The other pair of phasic cells could also be predicted by a (LWS + MWS) center and an opponent surround. However, the surround phase was 180° with respect to the center. All cells show a small center-surround latency.
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10

Ethier, C. Ross, Richie Abel, E. A. Sander, John G. Flanagan e Michael Girard. "Next-Generation Techniques for Analysis of Lamina Cribrosa Microstructure". In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80523.

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Glaucoma describes a group of potentially blinding ocular disorders, afflicting c. 60 million people worldwide. Of these, c. 8 million are bilaterally blind, estimated to increase to 11 million by 2020. The central event in glaucoma is slow and irreversible damage of retinal ganglion cells, responsible for carrying visual information from the retina to the brain (Figure 1). Intraocular pressure (IOP) is a risk factor for glaucoma1–4, and significant, sustained IOP reduction is unequivocally beneficial in the clinical management of glaucoma patients2, 3, 5. Unfortunately, we do not understand how elevated IOP leads to the loss of retinal ganglion cells.
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Rapporti di organizzazioni sul tema "Retinal ganglion cells"

1

Lugo-Garcia, N., R. E. Blanco e Ivonne Santiago. Characterization of Ground Squirrel Retinal Ganglion Cells. Fort Belvoir, VA: Defense Technical Information Center, dicembre 1990. http://dx.doi.org/10.21236/ada230311.

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