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Retinal Ganglion Cells

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (15 November 2019) | Viewed by 83675

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Dr. Marta Agudo-Barriuso

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Experimental Ophthalmology Group, Instituto Murciano de Investigación Biosanitaria Virgen de la Arrixaca (IMIB-Arrixaca) & Universidad de Murcia, 30120 Murcia, Spain
Interests: central nervous system; neuroprotection; neuroregeneration; neurodegeneration
Special Issues, Collections and Topics in MDPI journals

Dr. Ana Raquel Santiago

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Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, Coimbra, Portugal
Interests: retinal diseases; neuroprotection; neurodegeneration; neuroinflammation; neuro-immune interactions; drug delivery systems; intercellular communication; extracellular vesicles
Special Issues, Collections and Topics in MDPI journals

Dr. Eloisa Herrera

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Instituto de Neurociencias CSIC-UMH, Alicante, Spain
Interests: Development of neural circuits

Special Issue Information

Dear Colleagues,

This call for papers is focused on any aspect of retinal ganglion cells (RGCs) biology, during development and in adulthood. RGCs are highly specialized projection neurons. They are responsible for carrying the luminous information, visual and non-visual, from the retina to the brain.

A small proportion of RGCs express the photopigment melanopsin, rendering them intrinsically photosensitive and able to directly detect light. They send light irradiance information to the brain, and are responsible of the non-image forming responses to light, such as circadian photoentrainment or the pupillary reflex. Thus, there are two functional RGC types, image forming and non-image forming. Image-forming RGCs do not merely relay the luminous information, they extract different aspects of the image detecting light features, and thus, different RGC subtypes are specialized in specific light features.

Because the retina is part of the central nervous system RGC degeneration leads to an irrevocable loss of function which translates into blindness and dysregulation of the circadian rhythm. Current research aims to find the whys and hows behind RGC death in different pathophysiological scenarios, including the crosstalk of RGCs with glial cells, and much effort is being devoted to discover neuroprotective and neuroregenerative therapies.

The aim of this Special Issue is to update the current knowledge on RGCs, from the developmental cues that specify them to their response to injury.

You are warmly invited to submit original research, mini and full reviews, short communications, as well as perspectives, addressing any aspect of RGC biology.

Dr. Marta Agudo-Barriuso
Dr. Ana Raquel Santiago
Dr. Eloisa Herrera
Guest Editors

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

Retinal ganglion cells
Development
Visual system
Neuronal degeneration
Neuron-glia interactions
Animal models
Axonal regeneration
Retinal diseases
Therapy

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Published Papers (13 papers)

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Research

Jump to: Review

19 pages, 16693 KiB

Open AccessArticle

The mito-QC Reporter for Quantitative Mitophagy Assessment in Primary Retinal Ganglion Cells and Experimental Glaucoma Models

by Ines Rosignol, Beatriz Villarejo-Zori, Petra Teresak, Elena Sierra-Filardi, Xandra Pereiro, Natalia Rodríguez-Muela, Elena Vecino, Helena L. A. Vieira, Katharina Bell and Patricia Boya

Int. J. Mol. Sci. 2020, 21(5), 1882; https://doi.org/10.3390/ijms21051882 - 10 Mar 2020

Cited by 24 | Viewed by 7144

Abstract

Mitochondrial damage plays a prominent role in glaucoma. The only way cells can degrade whole mitochondria is via autophagy, in a process called mitophagy. Thus, studying mitophagy in the context of glaucoma is essential to understand the disease. Up to date limited tools are available for analyzing mitophagy in vivo. We have taken advantage of the mito-QC reporter, a recently generated mouse model that allows an accurate mitophagy assessment to fill this gap. We used primary RGCs and retinal explants derived from mito-QC mice to quantify mitophagy activation in vitro and ex vivo. We also analyzed mitophagy in retinal ganglion cells (RGCs), in vivo, using different mitophagy inducers, as well as after optic nerve crush (ONC) in mice, a commonly used surgical procedure to model glaucoma. Using mito-QC reporter we quantified mitophagy induced by several known inducers in primary RGCs in vitro, ex vivo and in vivo. We also found that RGCs were rescued from some glaucoma relevant stress factors by incubation with the iron chelator deferiprone (DFP). Thus, the mito-QC reporter-based model is a valuable tool for accurately analyzing mitophagy in the context of glaucoma. Full article

(This article belongs to the Special Issue Retinal Ganglion Cells)

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21 pages, 8048 KiB

Open AccessArticle

Neuronal Death in the Contralateral Un-Injured Retina after Unilateral Axotomy: Role of Microglial Cells

by Fernando Lucas-Ruiz, Caridad Galindo-Romero, Kristy T. Rodríguez-Ramírez, Manuel Vidal-Sanz and Marta Agudo-Barriuso

Int. J. Mol. Sci. 2019, 20(22), 5733; https://doi.org/10.3390/ijms20225733 - 15 Nov 2019

Cited by 26 | Viewed by 2703

Abstract

For years it has been known that unilateral optic nerve lesions induce a bilateral response that causes an inflammatory and microglial response in the contralateral un-injured retinas. Whether this contralateral response involves retinal ganglion cell (RGC) loss is still unknown. We have analyzed the population of RGCs and the expression of several genes in both retinas of pigmented mice after a unilateral axotomy performed close to the optic nerve head (0.5 mm), or the furthest away that the optic nerve can be accessed intraorbitally in mice (2 mm). In both retinas, RGC-specific genes were down-regulated, whereas caspase 3 was up-regulated. In the contralateral retinas, there was a significant loss of 15% of RGCs that did not progress further and that occurred earlier when the axotomy was performed at 2 mm, that is, closer to the contralateral retina. Finally, the systemic treatment with minocycline, a tetracycline antibiotic that selectively inhibits microglial cells, or with meloxicam, a non-steroidal anti-inflammatory drug, rescued RGCs in the contralateral but not in the injured retina. In conclusion, a unilateral optic nerve axotomy triggers a bilateral response that kills RGCs in the un-injured retina, a death that is controlled by anti-inflammatory and anti-microglial treatments. Thus, contralateral retinas should not be used as controls. Full article

(This article belongs to the Special Issue Retinal Ganglion Cells)

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22 pages, 4928 KiB

Open AccessArticle

Neuroprotective and Anti-Inflammatory Effects of a Hydrophilic Saffron Extract in a Model of Glaucoma

by Jose A. Fernández-Albarral, Ana I. Ramírez, Rosa de Hoz, Nerea López-Villarín, Elena Salobrar-García, Inés López-Cuenca, Ester Licastro, Antonio M. Inarejos-García, Paula Almodóvar, Maria D. Pinazo-Durán, José M. Ramírez and Juan J. Salazar

Int. J. Mol. Sci. 2019, 20(17), 4110; https://doi.org/10.3390/ijms20174110 - 22 Aug 2019

Cited by 60 | Viewed by 7355

Abstract

Glaucoma is a neurodegenerative disease characterized by the loss of retinal ganglion cells (RGCs). An increase in the intraocular pressure is the principal risk factor for such loss, but controlling this pressure does not always prevent glaucomatous damage. Activation of immune cells resident in the retina (microglia) may contribute to RGC death. Thus, a substance with anti-inflammatory activity may protect against RGC degeneration. This study investigated the neuroprotective and anti-inflammatory effects of a hydrophilic saffron extract standardized to 3% crocin content in a mouse model of unilateral, laser-induced ocular hypertension (OHT). Treatment with saffron extract decreased microglion numbers and morphological signs of their activation, including soma size and process retraction, both in OHT and in contralateral eyes. Saffron extract treatment also partially reversed OHT-induced down-regulation of P2RY12. In addition, the extract prevented retinal ganglion cell death in OHT eyes. Oral administration of saffron extract was able to decrease the neuroinflammation associated with increased intraocular pressure, preventing retinal ganglion cell death. Our findings indicate that saffron extract may exert a protective effect in glaucomatous pathology. Full article

(This article belongs to the Special Issue Retinal Ganglion Cells)

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14 pages, 4732 KiB

Open AccessArticle

A Chronic Ocular-Hypertensive Rat Model induced by Injection of the Sclerosant Agent Polidocanol in the Aqueous Humor Outflow Pathway

by Román Blanco, Gema Martinez-Navarrete, Consuelo Pérez-Rico, Francisco J. Valiente-Soriano, Marcelino Avilés-Trigueros, Javier Vicente, Eduardo Fernandez, Manuel Vidal-Sanz and Pedro de la Villa

Int. J. Mol. Sci. 2019, 20(13), 3209; https://doi.org/10.3390/ijms20133209 - 29 Jun 2019

Cited by 10 | Viewed by 3791

Abstract

Background: To induce a moderate chronic ocular hypertension (OHT) by injecting polidocanol, a foamed sclerosant drug, in the aqueous humor outflow pathway. Methods: Intraocular pressure (IOP) was monitored for up to 6 months. Pattern and full-field electroretinogram (PERG and ERG) were recorded and retinal ganglion cells (RGC) and retinal nerve fiber layer (RNFL) thickness were assessed in vivo with optical coherence tomography (OCT) and ex vivo using Brn3a immunohistochemistry. Results: In the first 3 weeks post-injection, a significant IOP elevation was observed in the treated eyes (18.47 ± 3.36 mmHg) when compared with the control fellow eyes (12.52 ± 2.84 mmHg) (p < 0.05). At 8 weeks, 65% (11/17) of intervention eyes had developed an IOP increase >25% over the baseline. PERG responses were seen to be significantly reduced in the hypertensive eyes (2.25 ± 0.24 µV) compared to control eyes (1.44 ± 0.19 µV) (p < 0.01) at week 3, whereas the ERG components (photoreceptor a-wave and bipolar cell b-wave) remained unaltered. By week 24, RNFL thinning and cell loss in the ganglion cell layer was first detected (2/13, 15.3%) as assessed by OCT and light microscopy. Conclusions: This novel OHT rat model, with moderate levels of chronically elevated IOP, and abnormal PERG shows selective functional impairment of RGC. Full article

(This article belongs to the Special Issue Retinal Ganglion Cells)

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21 pages, 3406 KiB

Open AccessArticle

Melanopsin⁺RGCs Are fully Resistant to NMDA-Induced Excitotoxicity

by Beatriz Vidal-Villegas, Johnny Di Pierdomenico, Juan A Miralles de Imperial-Ollero, Arturo Ortín-Martínez, Francisco M Nadal-Nicolás, Jose M Bernal-Garro, Nicolás Cuenca Navarro, María P Villegas-Pérez and Manuel Vidal-Sanz

Int. J. Mol. Sci. 2019, 20(12), 3012; https://doi.org/10.3390/ijms20123012 - 20 Jun 2019

Cited by 18 | Viewed by 4889

Abstract

We studied short- and long-term effects of intravitreal injection of N-methyl-d-aspartate (NMDA) on melanopsin-containing (m⁺) and non-melanopsin-containing (Brn3a⁺) retinal ganglion cells (RGCs). In adult SD-rats, the left eye received a single intravitreal injection of 5µL of 100nM NMDA. At 3 and 15 months, retinal thickness was measured in vivo using Spectral Domain-Optical Coherence Tomography (SD-OCT). Ex vivo analyses were done at 3, 7, or 14 days or 15 months after damage. Whole-mounted retinas were immunolabelled for brain-specific homeobox/POU domain protein 3A (Brn3a) and melanopsin (m), the total number of Brn3a⁺RGCs and m⁺RGCs were quantified, and their topography represented. In control retinas, the mean total numbers of Brn3a⁺RGCs and m⁺RGCs were 78,903 ± 3572 and 2358 ± 144 (mean ± SD; n = 10), respectively. In the NMDA injected retinas, Brn3a⁺RGCs numbers diminished to 49%, 28%, 24%, and 19%, at 3, 7, 14 days, and 15 months, respectively. There was no further loss between 7 days and 15 months. The number of immunoidentified m⁺RGCs decreased significantly at 3 days, recovered between 3 and 7 days, and were back to normal thereafter. OCT measurements revealed a significant thinning of the left retinas at 3 and 15 months. Intravitreal injections of NMDA induced within a week a rapid loss of 72% of Brn3a⁺RGCs, a transient downregulation of melanopsin expression (but not m⁺RGC death), and a thinning of the inner retinal layers. Full article

(This article belongs to the Special Issue Retinal Ganglion Cells)

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16 pages, 8188 KiB

Open AccessArticle

A Novel Reporter Mouse Uncovers Endogenous Brn3b Expression

by Adam M. Miltner, Yesica Mercado-Ayon, Simranjeet K. Cheema, Pengfei Zhang, Robert J. Zawadzki and Anna La Torre

Int. J. Mol. Sci. 2019, 20(12), 2903; https://doi.org/10.3390/ijms20122903 - 14 Jun 2019

Cited by 5 | Viewed by 5210

Abstract

Brn3b (Pou4f2) is a class-4 POU domain transcription factor known to play central roles in the development of different neuronal populations of the Central Nervous System, including retinal ganglion cells (RGCs), the neurons that connect the retina with the visual centers of the brain. Here, we have used CRISPR-based genetic engineering to generate a Brn3b-mCherry reporter mouse without altering the endogenous expression of Brn3b. In our mouse line, mCherry faithfully recapitulates normal Brn3b expression in the retina, the optic tracts, the midbrain tectum, and the trigeminal ganglia. The high sensitivity of mCherry also revealed novel expression of Brn3b in the neuroectodermal cells of the optic stalk during early stages of eye development. Importantly, the fluorescent intensity of Brn3b-mCherry in our reporter mice allows for noninvasive live imaging of RGCs using Scanning Laser Ophthalmoscopy (SLO), providing a novel tool for longitudinal monitoring of RGCs. Full article

(This article belongs to the Special Issue Retinal Ganglion Cells)

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Review

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23 pages, 815 KiB

Open AccessReview

Mechanisms behind Retinal Ganglion Cell Loss in Diabetes and Therapeutic Approach

by María Constanza Potilinski, Valeria Lorenc, Sofía Perisset and Juan Eduardo Gallo

Int. J. Mol. Sci. 2020, 21(7), 2351; https://doi.org/10.3390/ijms21072351 - 28 Mar 2020

Cited by 39 | Viewed by 5173

Abstract

Diabetes produces several changes in the body triggered by high glycemia. Some of these changes include altered metabolism, structural changes in blood vessels and chronic inflammation. The eye and particularly the retinal ganglion cells (RGCs) are not spared, and the changes eventually lead to cell loss and visual function impairment. Understanding the mechanisms resulting in RGC damage and loss from diabetic retinopathy is essential to find an effective treatment. This review focuses mainly on the signaling pathways and molecules involved in RGC loss and the potential therapeutic approaches for the prevention of this cell death. Throughout the manuscript it became evident that multiple factors of different kind are responsible for RGC damage. This shows that new therapeutic agents targeting several factors at the same time are needed. Alpha-1 antitrypsin as an anti-inflammatory agent may become a suitable option for the treatment of RGC loss because of its beneficial interaction with several signaling pathways involved in RGC injury and inflammation. In conclusion, alpha-1 antitrypsin may become a potential therapeutic agent for the treatment of RGC loss and processes behind diabetic retinopathy. Full article

(This article belongs to the Special Issue Retinal Ganglion Cells)

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39 pages, 5707 KiB

Open AccessReview

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

by Raquel Boia, Noelia Ruzafa, Inês Dinis Aires, Xandra Pereiro, António Francisco Ambrósio, Elena Vecino and Ana Raquel Santiago

Int. J. Mol. Sci. 2020, 21(7), 2262; https://doi.org/10.3390/ijms21072262 - 25 Mar 2020

Cited by 83 | Viewed by 11786

Abstract

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. Full article

(This article belongs to the Special Issue Retinal Ganglion Cells)

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24 pages, 2358 KiB

Open AccessReview

Neurogenesis and Specification of Retinal Ganglion Cells

by Kim Tuyen Nguyen-Ba-Charvet and Alexandra Rebsam

Int. J. Mol. Sci. 2020, 21(2), 451; https://doi.org/10.3390/ijms21020451 - 10 Jan 2020

Cited by 35 | Viewed by 9785

Abstract

Across all species, retinal ganglion cells (RGCs) are the first retinal neurons generated during development, followed by the other retinal cell types. How are retinal progenitor cells (RPCs) able to produce these cell types in a specific and timely order? Here, we will review the different models of retinal neurogenesis proposed over the last decades as well as the extrinsic and intrinsic factors controlling it. We will then focus on the molecular mechanisms, especially the cascade of transcription factors that regulate, more specifically, RGC fate. We will also comment on the recent discovery that the ciliary marginal zone is a new stem cell niche in mice contributing to retinal neurogenesis, especially to the generation of ipsilateral RGCs. Furthermore, RGCs are composed of many different subtypes that are anatomically, physiologically, functionally, and molecularly defined. We will summarize the different classifications of RGC subtypes and will recapitulate the specification of some of them and describe how a genetic disease such as albinism affects neurogenesis, resulting in profound visual deficits. Full article

(This article belongs to the Special Issue Retinal Ganglion Cells)

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16 pages, 6102 KiB

Open AccessReview

Retinal Ganglion Cell Death as a Late Remodeling Effect of Photoreceptor Degeneration

by Diego García-Ayuso, Johnny Di Pierdomenico, Manuel Vidal-Sanz and María P. Villegas-Pérez

Int. J. Mol. Sci. 2019, 20(18), 4649; https://doi.org/10.3390/ijms20184649 - 19 Sep 2019

Cited by 39 | Viewed by 4917

Abstract

Inherited or acquired photoreceptor degenerations, one of the leading causes of irreversible blindness in the world, are a group of retinal disorders that initially affect rods and cones, situated in the outer retina. For many years it was assumed that these diseases did not spread to the inner retina. However, it is now known that photoreceptor loss leads to an unavoidable chain of events that cause neurovascular changes in the retina including migration of retinal pigment epithelium cells, formation of “subretinal vascular complexes”, vessel displacement, retinal ganglion cell (RGC) axonal strangulation by retinal vessels, axonal transport alteration and, ultimately, RGC death. These events are common to all photoreceptor degenerations regardless of the initial trigger and thus threaten the outcome of photoreceptor substitution as a therapeutic approach, because with a degenerating inner retina, the photoreceptor signal will not reach the brain. In conclusion, therapies should be applied early in the course of photoreceptor degeneration, before the remodeling process reaches the inner retina. Full article

(This article belongs to the Special Issue Retinal Ganglion Cells)

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25 pages, 2324 KiB

Open AccessReview

Target-Derived Neurotrophic Factor Deprivation Puts Retinal Ganglion Cells on Death Row: Cold Hard Evidence and Caveats

by Marie Claes, Lies De Groef and Lieve Moons

Int. J. Mol. Sci. 2019, 20(17), 4314; https://doi.org/10.3390/ijms20174314 - 3 Sep 2019

Cited by 15 | Viewed by 5311

Abstract

Glaucoma and other optic neuropathies are characterized by axonal transport deficits. Axonal cargo travels back and forth between the soma and the axon terminus, a mechanism ensuring homeostasis and the viability of a neuron. An example of vital molecules in the axonal cargo are neurotrophic factors (NTFs). Hindered retrograde transport can cause a scarcity of those factors in the retina, which in turn can tilt the fate of retinal ganglion cells (RGCs) towards apoptosis. This postulation is one of the most widely recognized theories to explain RGC death in the disease progression of glaucoma and is known as the NTF deprivation theory. For several decades, research has been focused on the use of NTFs as a novel neuroprotective glaucoma treatment. Until now, results in animal models have been promising, but translation to the clinic has been highly disappointing. Are we lacking important knowledge to lever NTF therapies towards the therapeutic armamentarium? Or did we get the wrong end of the stick regarding the NTF deprivation theory? In this review, we will tackle the existing evidence and caveats advocating for and against the target-derived NTF deprivation theory in glaucoma, whilst digging into associated therapy efforts. Full article

(This article belongs to the Special Issue Retinal Ganglion Cells)

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21 pages, 1256 KiB

Open AccessReview

Wiring the Binocular Visual Pathways

by Verónica Murcia-Belmonte and Lynda Erskine

Int. J. Mol. Sci. 2019, 20(13), 3282; https://doi.org/10.3390/ijms20133282 - 4 Jul 2019

Cited by 29 | Viewed by 7424

Abstract

Retinal ganglion cells (RGCs) extend axons out of the retina to transmit visual information to the brain. These connections are established during development through the navigation of RGC axons along a relatively long, stereotypical pathway. RGC axons exit the eye at the optic disc and extend along the optic nerves to the ventral midline of the brain, where the two nerves meet to form the optic chiasm. In animals with binocular vision, the axons face a choice at the optic chiasm—to cross the midline and project to targets on the contralateral side of the brain, or avoid crossing the midline and project to ipsilateral brain targets. Ipsilaterally and contralaterally projecting RGCs originate in disparate regions of the retina that relate to the extent of binocular overlap in the visual field. In humans virtually all RGC axons originating in temporal retina project ipsilaterally, whereas in mice, ipsilaterally projecting RGCs are confined to the peripheral ventrotemporal retina. This review will discuss recent advances in our understanding of the mechanisms regulating specification of ipsilateral versus contralateral RGCs, and the differential guidance of their axons at the optic chiasm. Recent insights into the establishment of congruent topographic maps in both brain hemispheres also will be discussed. Full article

(This article belongs to the Special Issue Retinal Ganglion Cells)

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18 pages, 4487 KiB

Open AccessReview

Photosensitive Melanopsin-Containing Retinal Ganglion Cells in Health and Disease: Implications for Circadian Rhythms

by Pedro Lax, Isabel Ortuño-Lizarán, Victoria Maneu, Manuel Vidal-Sanz and Nicolás Cuenca

Int. J. Mol. Sci. 2019, 20(13), 3164; https://doi.org/10.3390/ijms20133164 - 28 Jun 2019

Cited by 48 | Viewed by 7060

Abstract

Melanopsin-containing retinal ganglion cells (mRGCs) represent a third class of retinal photoreceptors involved in regulating the pupillary light reflex and circadian photoentrainment, among other things. The functional integrity of the circadian system and melanopsin cells is an essential component of well-being and health, being both impaired in aging and disease. Here we review evidence of melanopsin-expressing cell alterations in aging and neurodegenerative diseases and their correlation with the development of circadian rhythm disorders. In healthy humans, the average density of melanopsin-positive cells falls after age 70, accompanied by age-dependent atrophy of dendritic arborization. In addition to aging, inner and outer retinal diseases also involve progressive deterioration and loss of mRGCs that positively correlates with progressive alterations in circadian rhythms. Among others, mRGC number and plexus complexity are impaired in Parkinson’s disease patients; changes that may explain sleep and circadian rhythm disorders in this pathology. The key role of mRGCs in circadian photoentrainment and their loss in age and disease endorse the importance of eye care, even if vision is lost, to preserve melanopsin ganglion cells and their essential functions in the maintenance of an adequate quality of life. Full article

(This article belongs to the Special Issue Retinal Ganglion Cells)

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