scholarly journals The statistics of looking: Deriving properties of retinal ganglion cells across the visual field

2012 ◽  
Vol 12 (9) ◽  
pp. 771-771
Author(s):  
D. Pamplona ◽  
J. Triesch ◽  
C. A. Rothkopf
Keyword(s):  
Visual Field ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion

scholarly journals The Relationship between Visual Field Index and Estimated Number of Retinal Ganglion Cells in Glaucoma

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e76590 ◽  
Author(s):  
Amir H. Marvasti ◽  
Andrew J. Tatham ◽  
Linda M. Zangwill ◽  
Christopher A. Girkin ◽  
Jeffrey M. Liebmann ◽  
...  
Keyword(s):  
Visual Field ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Visual Field Index ◽  
The Relationship

Design of Experiments for Exposure of Astrocytes to Elevated Hydrostatic Pressure and Hypoxia

2008 ◽  
Author(s):  
Shadi Rajabi ◽  
Craig A. Simmons ◽  
C. Ross Ethier
Keyword(s):  
Intraocular Pressure ◽  
Visual Field ◽  
Retinal Ganglion Cells ◽  
Vision Loss ◽  
Ganglion Cells ◽  
Visual Field Loss ◽  
Retinal Ganglion ◽  
Common Cause ◽  
Elevated Intraocular Pressure

Glaucoma, a chronic optic neuropathy, is the second most common cause of blindness, affecting 67 million people worldwide. The damage in glaucoma occurs at the optic nerve head (ONH), where the axons of the retinal ganglion cells leave the eye posteriorly. Glaucoma is frequently associated with elevated intraocular pressure (IOP), and visual field loss can be prevented by significant lowering of IOP. Hence, the role of pressure in glaucoma is important. Unfortunately, the mechanism by which pressure leads to vision loss in glaucoma is very poorly understood.

Visual field defects in cats with neonatal or adult immunological loss of retinal ganglion cells

1986 ◽  
Vol 368 (1) ◽  
pp. 154-157 ◽  
Author(s):  
Peter D. Spear ◽  
Stephanie Miller ◽  
Kathleen Vielhuber ◽  
Steven E. Kornguth
Keyword(s):  
Visual Field ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Visual Field Defects ◽  
Retinal Ganglion ◽  
Field Defects

scholarly journals Dual SMAD inhibition and Wnt inhibition enable efficient and reproducible differentiations of induced pluripotent stem cells into retinal ganglion cells

2019 ◽  
Author(s):  
Venkata R. M. Chavali ◽  
Naqi Haider ◽  
Sonika Rathi ◽  
Vrathasha Vrathasha ◽  
Teja Alapati ◽  
...  
Keyword(s):  
Stem Cells ◽  
Optic Nerve ◽  
Visual Field ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Visual Field Loss ◽  
Nerve Degeneration ◽  
Retinal Ganglion

AbstractGlaucoma is a group of progressive optic neuropathies that share common biological and clinical characteristics including irreversible changes to the optic nerve and visual field loss caused by death of retinal ganglion cells (RGCs). The loss of RGCs manifests as characteristic cupping or optic nerve degeneration, resulting in visual field loss in patients with Glaucoma. Published studies on in vitro RGC differentiation from stem cells utilized classical RGC signaling pathways mimicking retinal development in vivo. Although many strategies allowed for the generation of RGCs, increased variability between experiments and lower yield hampered the cross comparison between individual lines and between experiments. To address this critical need, we developed a reproducible chemically defined in vitro methodology for generating retinal progenitor cell (RPC) populations from iPSCs, that are efficiently directed towards RGC lineage. Using this method, we reproducibly differentiated iPSCs into RGCs with greater than 80% purity, without any genetic modifications. We used small molecules and peptide modulators to inhibit BMP, TGF-β (SMAD), and canonical Wnt pathways that reduced variability between iPSC lines and yielded functional and mature iPSC-RGCs. Using CD90.2 antibody and Magnetic Activated Cell Sorter (MACS) technique, we successfully purified Thy-1 positive RGCs with nearly 95% purity.

scholarly journals Survival of retinal ganglion cells after damage to the occipital lobe in humans is activity dependent

2019 ◽  
Vol 286 (1897) ◽  
pp. 20182733 ◽  
Author(s):  
Colleen L. Schneider ◽  
Emily K. Prentiss ◽  
Ania Busza ◽  
Kelly Matmati ◽  
Nabil Matmati ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Visual Field ◽  
Ganglion Cell ◽  
Retinal Ganglion Cells ◽  
Retinal Ganglion Cell ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Cell Degeneration ◽  
Visual Ability ◽  
Activity Dependent

Damage to the optic radiations or primary visual cortex leads to blindness in all or part of the contralesional visual field. Such damage disconnects the retina from its downstream targets and, over time, leads to trans-synaptic retrograde degeneration of retinal ganglion cells. To date, visual ability is the only predictor of retinal ganglion cell degeneration that has been investigated after geniculostriate damage. Given prior findings that some patients have preserved visual cortex activity for stimuli presented in their blind field, we tested whether that activity explains variability in retinal ganglion cell degeneration over and above visual ability. We prospectively studied 15 patients (four females, mean age = 63.7 years) with homonymous visual field defects secondary to stroke, 10 of whom were tested within the first two months after stroke. Each patient completed automated Humphrey visual field testing, retinotopic mapping with functional magnetic resonance imaging, and spectral-domain optical coherence tomography of the macula. There was a positive relation between ganglion cell complex (GCC) thickness in the blind field and early visual cortex activity for stimuli presented in the blind field. Furthermore, residual visual cortex activity for stimuli presented in the blind field soon after the stroke predicted the degree of retinal GCC thinning six months later. These findings indicate that retinal ganglion cell survival after ischaemic damage to the geniculostriate pathway is activity dependent.

scholarly journals Wiring the Binocular Visual Pathways

2019 ◽  
Vol 20 (13) ◽  
pp. 3282 ◽  
Author(s):  
Verónica Murcia-Belmonte ◽  
Lynda Erskine
Keyword(s):  
Visual Field ◽  
Retinal Ganglion Cells ◽  
Visual Information ◽  
Ganglion Cells ◽  
Optic Chiasm ◽  
Contralateral Side ◽  
Topographic Maps ◽  
Retinal Ganglion ◽  
Brain Hemispheres ◽  
The Brain

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.

scholarly journals Improvement in Inner Retinal Function in Glaucoma in Response to Nicotinamide (Vitamin B3) Supplementation: A Crossover Randomized Clinical Trial

2020 ◽  
Author(s):  
Flora Hui ◽  
Jessica Tang ◽  
Pete A Williams ◽  
Myra B McGuinness ◽  
Xavier Hadoux ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Visual Field ◽  
Ganglion Cell ◽  
Retinal Ganglion Cells ◽  
Cell Function ◽  
Ganglion Cells ◽  
Retinal Function ◽  
Trial Registration ◽  
Retinal Ganglion ◽  
Retinal Ganglion Cell Function

AbstractImportanceRetinal ganglion cells endure significant metabolic stress with ageing and glaucoma-related stressors. Injured cells require increased energy for repair but maintain capacity to recover function despite periods of functional loss. Nicotinamide, a precursor of redox co-factor and metabolite, NAD+, is low in serum of patients with primary open-angle glaucoma and its supplementation provides robust protection of retinal ganglion cells by targeting mitochondrial health in glaucoma models. However, the potential of nicotinamide to improve retinal ganglion cell function in humans with glaucoma is yet unknown.ObjectiveTo determine whether nicotinamide supplementation taken in conjunction with conventional IOP-lowering therapy leads to early improvement in retinal ganglion cell function in people with glaucoma.DesignCrossover, double-masked, randomized clinical trial conducted between October 2017 to January 2019.SettingStudy participants recruited from two tertiary care centers in Melbourne, Australia.ParticipantsAdults diagnosed and treated for primary glaucoma. Ninety-four participants assessed for study eligibility.InterventionParticipants randomized to first receive oral placebo or nicotinamide and reviewed six-weekly. Accelerated dosing method utilized; participants commenced 6-week course of 1.5 grams/day followed by 6 weeks of 3.0 grams/day. After 12 weeks, participants crossed over to other intervention for 12 weeks without washout. At each visit, visual function measured using full-field flash electroretinography and white-on-white perimetry.Main outcome measuresPrimary endpoint was change in inner retinal function determined a-priori as change in photopic negative response (PhNR) parameters: saturated PhNR amplitude (Vmax), ratio of PhNR/b-wave amplitude (Vmax ratio).ResultsFifty-seven participants (65.5±10.0 years, 39% female) enrolled. PhNR Vmax improved beyond 95% coefficient of repeatability (COR) in 23% of participants following 12 weeks of nicotinamide versus 9% on placebo. Conversely, PhNR Vmax deteriorated in 9% on placebo and 7% on nicotinamide. Overall, Vmax improved by 14.8% [95% CI: 2.8%, 26.9%], (p=0.02) on nicotinamide and 5.2% [-4.2%, 14.6%], (p=0.27) on placebo. Vmax ratio improved on average by 12.6% [5.0%, 20.2%], (p=0.002) following nicotinamide and 3.6% [-3.4%, 10.5%], (p=0.30) on placebo. A concomitant trend for improved visual field mean deviation was observed with 27% improving ≥1dB on nicotinamide and fewer deteriorating ≥1dB (4%) compared to placebo (p=0.02). Moderate correlation was observed between PhNR and visual field change with treatment. Participants demonstrated excellent treatment adherence rates (>94%) and nicotinamide was well tolerated with minimal side effects.Conclusions and RelevanceNicotinamide supplementation can improve inner retinal function in patients receiving concurrent IOP-lowering glaucoma therapy. Further studies are underway to elucidate the effects of long-term nicotinamide supplementation on glaucoma progression.Trial RegistrationANZCTR trial ID: ACTRN12617000809336 https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=373001

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