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Advances in Visual Neuroscience

A special issue of Applied Sciences (ISSN 2076-3417). This special issue belongs to the section "Applied Neuroscience and Neural Engineering".

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 1423

Special Issue Editor


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Guest Editor
Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, 67100 L'Aquila, Italy
Interests: retina; neurodegeneration; neuroprotection; retinal pigment epithelium; retinal function; age related macular degeneration; retinal organoids; hESCs; iPSCs
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Visual neuroscience is a branch of neuroscience that focuses on the visual system of the human body, mainly located in the eye and brain’s visual cortex. The main goal of visual neuroscience is to understand how neural activity results in the final visual perception, from the time when light stimuli hit the retina to the visual perception of the surroundings. Vision perception is a sense related to retinal function, where retinal photoreceptors, bipolar and horizontal cells, and retinal ganglion cells that form the optic nerve are interconnected and supported by the retinal pigment epithelium and the downstream neurons in the visual cortex.

This Special Issue will cover recent research advances in all aspects of vision neurosciences.

In particular, the topics of interest include, but are not limited to:

  • Visual system;
  • Visual impairment;
  • Visual disfunction;
  • Blindness;
  • Neurophysiology;
  • Sensory system;
  • Eye;
  • Retinal development;
  • Retinal organoid;
  • Photoreceptors;
  • Cell therapies, including stem cell therapy;
  • Optogenetics;
  • Gene therapy.

Dr. Darin Zerti
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2400 CHF (Swiss Francs). 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

  • retina
  • neurodegeneration
  • ophthalmology
  • vision
  • neurosciences
  • neuroprotection

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Published Papers (1 paper)

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Research

12 pages, 2523 KiB  
Article
Myo/Nog Cells Increase in Response to Elevated Intraocular Pressure and Mitigate Ganglion Cell Death in a Mouse Model of Glaucoma
by Paul Lecker, Karanveer Johal, Alexa McGrath, John Spikes II, Jake Bernstein, Victoria MacPherson, Rushil Brahmbhatt, Nada Fadl, Edgar Weyback-Liogier, Sarah Adams, Rachel Souza, E-Jine Tsai, Mark Martin, Jacquelyn Gerhart, Grezgorz Gorski, Federica De Cecco, Brian Heist, Sebastian Egberts, Mindy George-Weinstein and Arturo Bravo-Nuevo
Appl. Sci. 2023, 13(22), 12423; https://doi.org/10.3390/app132212423 - 17 Nov 2023
Viewed by 1037
Abstract
Glaucoma is one of the leading causes of blindness worldwide. Decreased aqueous humor drainage causes an increase in intraocular pressure (IOP), which in turn damages the ganglion cells of the retina and optic nerve. A mouse model of glaucoma was used to examine [...] Read more.
Glaucoma is one of the leading causes of blindness worldwide. Decreased aqueous humor drainage causes an increase in intraocular pressure (IOP), which in turn damages the ganglion cells of the retina and optic nerve. A mouse model of glaucoma was used to examine the behavior of Myo/Nog (M/N) cells, which were previously shown to respond to cataract surgery and retinopathy induced by hypoxia, light damage, and intravitreal injection of human retinal pigment epithelial cells. M/N cells express the skeletal-muscle-specific transcription factor MyoD, the bone morphogenetic protein inhibitor Noggin, and brain-specific angiogenesis inhibitor 1 (BAI1). Glaucoma was induced by injecting microbeads into the anterior chamber (AC) of the right eye to obstruct the flow of aqueous humor into the trabecular meshwork. IOP was elevated within three days of addition of microbeads. Loss of retinal ganglion cells (RGCs) and thinning of the ganglion cell layer–nerve fiber layer (GCL-NFL) was observed in tissue sections by day 32. The injection of microbeads resulted in an increase in BAI1-positive (+) M/N cells in the trabecular meshwork, ciliary body, canal of Schlemm, cornea, and ganglion cell layer (GCL). M/N cells ingested microbeads. The effect of further increasing the population of M/N cells on IOP and RGC loss was determined by injecting BAI1+ cells isolated from the brain into the AC of both eyes. Exogenous M/N cells prelabeled with CellTracker™ Red were found in the same tissues as the endogenous population of M/N cells in eyes with and without elevated IOP. The addition of M/N cells did not significantly reduce IOP in bead-injected eyes. However, there were significantly more RGCs and the NFL was thicker in glaucomatous eyes with M/N cell supplementation than eyes injected with phosphate-buffered saline. The numbers of RGCs and NFL thickness were similar in glaucomatous and non-glaucomatous eyes after adding M/N cells. These results demonstrate that endogenous M/N cells respond to elevated IOP in the anterior and posterior segments in response to induction of glaucoma. M/N cells’ mitigation of RGC loss may reflect a neuroprotective effect within the retina, as opposed to a significant drop in IOP. Full article
(This article belongs to the Special Issue Advances in Visual Neuroscience)
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