Shared and Differential Retinal Responses against Optic Nerve Injury and Ocular Hypertension

Vidal‐Sanz, Manuel; Galindo‐Romero, Caridad; Valiente‐Soriano, Francisco J.; Nadal-Nicolás, Francisco M.; Ortín-Martínez, Arturo; Rovere, Giuseppe; Salinas‐Navarro, Manuel; Lucas‐Ruiz, Fernando; Sánchez-Migallón, M.C.; Sobrado‐Calvo, Paloma; Avilés‐Trigueros, Marcelino; Villegas‐Pérez, María Paz; Agudo‐Barriuso, Marta

doi:10.3389/fnins.2017.00235

Cited by 83 publications

(86 citation statements)

References 115 publications

(250 reference statements)

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“…19,[27][28][29][30][31] Retinal multiframe acquisitions of the whole retinas were acquired in a raster scan pattern using a 310 objective (Plan-Neofluar, 103/ 0.30; Zeiss Mikroskopie). Every single frame was focused manually before acquisition of the image.…”

Section: Retinal Image Analysis Quantification and Distribution Ofmentioning

confidence: 99%

Taurine Depletion Causes ipRGC Loss and Increases Light-Induced Photoreceptor Degeneration

García‐Ayuso

Pierdomenico

Hadj-Saïd

et al. 2018

Invest. Ophthalmol. Vis. Sci.

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METHODS. Albino rats received b-alanine in the drinking water to induce taurine depletion. One month later, half of the animals were exposed to white light (3000 lux) continuously for 48 hours and the rest remained in normal environmental conditions. A control group of animals nontreated with b-alanine also was prepared, and half of them were exposed to light using the same protocol. All the animals were processed 2 months after the beginning of the experiment. Retinas were dissected as wholemounts and immunodetected with antibodies against Brn3a, melanopsin, S-opsin, and L-opsin to label different retinal populations: Brn3a þ retinal ganglion cells (RGCs) (image-forming RGCs), m þ RGCs (non-image-forming RGCs), and S-and L/M-cones, respectively. RESULTS. Light exposure did not affect the numbers of Brn3aþ RGCs or m þ RGCs but diminished the numbers of S-and L/M-cones and caused the appearance of rings devoid of cones, mainly in an ''arciform'' area in the superotemporal retina. Taurine depletion caused a diminution of all the studied populations, with m þ RGCs the most affected, followed by Scones. Light exposure under taurine depletion increased photoreceptor degeneration but did not seem to increase Brn3a þ RGCs or m þ RGCs loss. CONCLUSIONS.Our results document that taurine is necessary for cell survival in the rat retina and even more under light-induced photoreceptor degeneration. Thus, taurine supplementation may help to prevent retinal degenerations, especially those that commence with S-cone degeneration or in which light may be an etiologic factor, such as inherited retinal degenerations, AMD, or glaucoma.

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Section: Retinal Image Analysis Quantification and Distribution Ofmentioning

confidence: 99%

Taurine Depletion Causes ipRGC Loss and Increases Light-Induced Photoreceptor Degeneration

García‐Ayuso

Pierdomenico

Hadj-Saïd

et al. 2018

Invest. Ophthalmol. Vis. Sci.

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“…23 In addition, ipRGCs show high resistance to optic nerve transection or crush, glutamate neurotoxicity, and acute ocular hypertension, but not to chronic ocular hypertension, suggesting that ipRGCs respond differently among injuries. [24][25][26] Glaucoma usually is associated with increased IOP, but a subset of glaucoma presents with statistically normal IOP, called normal tension glaucoma (NTG), suggesting the possibility that non-IOP-dependent factors may contribute to the disease progression. 27,28 We previously reported that loss of glutamate/aspartate transporter (GLAST) in mice leads to progressive RGC loss and optic nerve degeneration while maintaining normal IOP, demonstrating key pathologic features of NTG.…”

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confidence: 99%

Survival of Alpha and Intrinsically Photosensitive Retinal Ganglion Cells in NMDA-Induced Neurotoxicity and a Mouse Model of Normal Tension Glaucoma

Honda

Namekata

Kimura

et al. 2019

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. We assess if a retinal ganglion cells (aRGCs) and intrinsically photosensitive retinal ganglion cells (ipRGCs) survive in mouse models of glaucoma. METHODS. Two microliters of N-methyl-D-aspartate (NMDA; 1 mM) or PBS were injected intraocularly 7 days before sacrifice. Immunohistochemical analyses of the retina were performed using antibodies against RNA-binding protein with multiple splicing (RBPMS), osteopontin, and melanopsin. Immunohistochemical analyses also were performed in adult mice with glutamate/aspartate transporter (GLAST) deletion (GLAST knockout [KO] mice), a mouse model of normal tension glaucoma. RESULTS. NMDA-induced loss of RBPMS-positive total RGCs was 58.4% 6 0.4% compared to PBS-treated controls, whereas the loss of osteopontin-positive aRGCs was 5.0% 6 0.6% and that of melanopsin-positive ipRGCs was 7.6% 6 1.6%. In GLAST KO mice, the loss of total RGCs was 48.4% 6 0.9% compared to wild-type mice, whereas the loss of aRGCs and ipRGCs was 3.9% 6 0.4% and 9.3% 6 0.5%, respectively. The distribution of survived total RGCs, aRGCs, and ipRGCs was similar regardless of the location of the retina. CONCLUSIONS. These results suggest that aRGC and ipRGC are highly tolerant to NMDA-induced neurotoxicity and NTG-like neurodegeneration in GLAST KO mice.

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“…It has been shown that non-image forming ipRGCs exhibited a preferential survival following injury compared to image forming RGCs. This fact was observed in different injury and disease models, demonstrating the resilience to damage of this subtype of RGCs [326]. ipRGCs have the ability to respond to light using the photopigment melanopsin, and they play a role in circadian rhythms and pupillary reflexes through their projections to the suprachiasmatic nucleus and the olivary pretectal nucleus [327].…”

Section: Different Types Of Rgcs and Their Susceptibility After Retinmentioning

confidence: 85%

Neuroprotective Strategies for Retinal Ganglion Cell Degeneration: Current Status and Challenges Ahead

Boia

Ruzafa

Aires

et al. 2020

IJMS

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The retinal ganglion cells (RGCs) are the output cells of the retina into the brain. In mammals, these cells are not able to regenerate their axons after optic nerve injury, leaving the patients with optic neuropathies with permanent visual loss. An effective RGCs-directed therapy could provide a beneficial effect to prevent the progression of the disease. Axonal injury leads to the functional loss of RGCs and subsequently induces neuronal death, and axonal regeneration would be essential to restore the neuronal connectivity, and to reestablish the function of the visual system. The manipulation of several intrinsic and extrinsic factors has been proposed in order to stimulate axonal regeneration and functional repairing of axonal connections in the visual pathway. However, there is a missing point in the process since, until now, there is no therapeutic strategy directed to promote axonal regeneration of RGCs as a therapeutic approach for optic neuropathies.

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Shared and Differential Retinal Responses against Optic Nerve Injury and Ocular Hypertension

Cited by 83 publications

References 115 publications

Taurine Depletion Causes ipRGC Loss and Increases Light-Induced Photoreceptor Degeneration

Taurine Depletion Causes ipRGC Loss and Increases Light-Induced Photoreceptor Degeneration

Survival of Alpha and Intrinsically Photosensitive Retinal Ganglion Cells in NMDA-Induced Neurotoxicity and a Mouse Model of Normal Tension Glaucoma

Neuroprotective Strategies for Retinal Ganglion Cell Degeneration: Current Status and Challenges Ahead

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