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Retinal Ganglion Cells 2.0
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Retinal Ganglion Cells 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (15 May 2021) | Viewed by 8290

Special Issue Editor

Dr. Marta Agudo-Barriuso

E-Mail Website
Guest Editor
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

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
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

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

Published Papers (3 papers)

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Research

19 pages, 53520 KiB  
Article
Red Light Irradiation In Vivo Upregulates DJ-1 in the Retinal Ganglion Cell Layer and Protects against Axotomy-Related Dendritic Pruning
by Kathy Beirne, Thomas J. Freeman, Malgorzata Rozanowska and Marcela Votruba
Int. J. Mol. Sci. 2021, 22(16), 8380; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22168380 - 04 Aug 2021
Cited by 3 | Viewed by 2017
Abstract
Retinal ganglion cells (RGCs) undergo dendritic pruning in a variety of neurodegenerative diseases, including glaucoma and autosomal dominant optic atrophy (ADOA). Axotomising RGCs by severing the optic nerve generates an acute model of RGC dendropathy, which can be utilized to assess the therapeutic [...] Read more.
Retinal ganglion cells (RGCs) undergo dendritic pruning in a variety of neurodegenerative diseases, including glaucoma and autosomal dominant optic atrophy (ADOA). Axotomising RGCs by severing the optic nerve generates an acute model of RGC dendropathy, which can be utilized to assess the therapeutic potential of treatments for RGC degeneration. Photobiomodulation (PBM) with red light provided neuroprotection to RGCs when administered ex vivo to wild-type retinal explants. In the current study, we used aged (13–15-month-old) wild-type and heterozygous B6;C3-Opa1Q285STOP (Opa1+/−) mice, a model of ADOA exhibiting RGC dendropathy. These mice were pre-treated with 4 J/cm2 of 670 nm light for five consecutive days before the eyes were enucleated and the retinas flat-mounted into explant cultures for 0-, 8- or 16-h ex vivo. RGCs were imaged by confocal microscopy, and their dendritic architecture was quantified by Sholl analysis. In vivo 670 nm light pretreatment inhibited the RGC dendropathy observed in untreated wild-type retinas over 16 h ex vivo and inhibited dendropathy in ON-center RGCs in wild-type but not Opa1+/− retinas. Immunohistochemistry revealed that aged Opa1+/− RGCs exhibited increased nitrosative damage alongside significantly lower activation of NF-κB and upregulation of DJ-1. PBM restored NF-κB activation in Opa1+/− RGCs and enhanced DJ-1 expression in both genotypes, indicating a potential molecular mechanism priming the retina to resist future oxidative insult. These data support the potential of PBM as a treatment for diseases involving RGC degeneration. Full article
(This article belongs to the Special Issue Retinal Ganglion Cells 2.0)
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18 pages, 2103 KiB  
Article
A Fair Assessment of Evaluation Tools for the Murine Microbead Occlusion Model of Glaucoma
by Marie Claes, Joana R. F. Santos, Luca Masin, Lien Cools, Benjamin M. Davis, Lutgarde Arckens, Karl Farrow, Lies De Groef and Lieve Moons
Int. J. Mol. Sci. 2021, 22(11), 5633; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22115633 - 26 May 2021
Cited by 4 | Viewed by 3007
Abstract
Despite being one of the most studied eye diseases, clinical translation of glaucoma research is hampered, at least in part, by the lack of validated preclinical models and readouts. The most popular experimental glaucoma model is the murine microbead occlusion model, yet the [...] Read more.
Despite being one of the most studied eye diseases, clinical translation of glaucoma research is hampered, at least in part, by the lack of validated preclinical models and readouts. The most popular experimental glaucoma model is the murine microbead occlusion model, yet the observed mild phenotype, mixed success rate, and weak reproducibility urge for an expansion of available readout tools. For this purpose, we evaluated various measures that reflect early onset glaucomatous changes in the murine microbead occlusion model. Anterior chamber depth measurements and scotopic threshold response recordings were identified as an outstanding set of tools to assess the model’s success rate and to chart glaucomatous damage (or neuroprotection in future studies), respectively. Both are easy-to-measure, in vivo tools with a fast acquisition time and high translatability to the clinic and can be used, whenever judged beneficial, in combination with the more conventional measures in present-day glaucoma research (i.e., intraocular pressure measurements and post-mortem histological analyses). Furthermore, we highlighted the use of dendritic arbor analysis as an alternative histological readout for retinal ganglion cell density counts. Full article
(This article belongs to the Special Issue Retinal Ganglion Cells 2.0)
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Graphical abstract

14 pages, 2448 KiB  
Article
Structure–Function Relationship of Retinal Ganglion Cells in Multiple Sclerosis
by Khaldoon O. Al-Nosairy, Marc Horbrügger, Sven Schippling, Markus Wagner, Aiden Haghikia, Marc Pawlitzki and Michael B. Hoffmann
Int. J. Mol. Sci. 2021, 22(7), 3419; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073419 - 26 Mar 2021
Cited by 5 | Viewed by 2560
Abstract
The retinal ganglion cells (RGC) may be considered an easily accessible pathophysiological site of degenerative processes in neurological diseases, such as the RGC damage detectable in multiple sclerosis (MS) patients with (HON) and without a history of optic neuritis (NON). We aimed to [...] Read more.
The retinal ganglion cells (RGC) may be considered an easily accessible pathophysiological site of degenerative processes in neurological diseases, such as the RGC damage detectable in multiple sclerosis (MS) patients with (HON) and without a history of optic neuritis (NON). We aimed to assess and interrelate RGC functional and structural damage in different retinal layers and retinal sites. We included 12 NON patients, 11 HON patients and 14 healthy controls for cross-sectional multifocal pattern electroretinography (mfPERG) and optical coherence tomography (OCT) measurements. Amplitude and peak times of the mfPERG were assessed. Macula and disc OCT scans were acquired to determine macular retinal layer and peripapillary retinal nerve fiber layer (pRNFL) thickness. In both HON and NON patients the foveal N2 amplitude of the mfPERG was reduced compared to controls. The parafoveal P1 peak time was significantly reduced in HON only. For OCT, parafoveal (pfGCL) and perifoveal (pGCL) ganglion cell layer thicknesses were decreased in HON vs. controls, while pRNFL in the papillomacular bundle sector (PMB) showed reductions in both NON and HON. As the mfPERG derived N2 originates from RGC axons, these findings suggest foveal axonal dysfunction not only in HON, but also in NON patients. Full article
(This article belongs to the Special Issue Retinal Ganglion Cells 2.0)
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