scholarly journals Visual Perception in the Periphery: The Role of Covert Attention Vectors in the Extraction of Semantic Information

2020 ◽  
Author(s):  
Ikaasa Suri ◽  
Patrick McGranor Wilson ◽  
Saba Doustmohammadi ◽  
Anna De Schutter ◽  
Thida Sandy Chunwatanapong ◽  
...  
Keyword(s):  
Visual Perception ◽  
Semantic Information ◽  
Ganglion Cells ◽  
Covert Attention ◽  
Retinal Ganglion ◽  
Scale Invariant ◽  
Dorsal Pathway ◽  
Ventral Pathway ◽  
Foveal Center

AbstractUnder covert attention, our visual perception deteriorates dramatically as eccentricity increases. This reduction of peripheral visual acuity (PVA) is partially due to the coarse sampling of the retinal ganglion cells towards the periphery, but this property cannot be solely responsible. Other factors, such as character crowding, have been studied, yet the origin of the poor PVA is not entirely understood. This gap motivated us to investigate the PVA by varying the crowding conditions systematically. Under completely crowded conditions (i.e. resembling a full page of text), PVA was observed to be eight times worse than the PVA under uncrowded conditions. By partially crowding the periphery, we obtained PVA values between the fully crowded and uncrowded conditions. On the other hand, crowding the fovea center while leaving the periphery uncrowded improved PVA relative to the uncrowded case. These results support a model for a top-down “covert attention vector” that assists the resulting PVA in a manner analogous to saccadic eye movement for overt attention. We speculate that the attention vector instructs the dorsal pathway to transform the peripheral character to the foveal center. Then, the scale-invariant log-polar retinotopy of the ventral pathway can scale the centered visual input to match the prior memory of the specific character shape.

scholarly journals Endothelin 1-induced retinal ganglion cell death is largely mediated by JUN activation

2020 ◽  
Vol 11 (9) ◽  
Author(s):  
Olivia J. Marola ◽  
Stephanie B. Syc-Mazurek ◽  
Gareth R. Howell ◽  
Richard T. Libby
Keyword(s):  
Transcription Factor ◽  
Molecular Mechanisms ◽  
Ganglion Cells ◽  
Retinal Vessel ◽  
Vessel Diameter ◽  
Retinal Ganglion ◽  
Retinal Ganglion Cell Death ◽  
Ganglion Cell Death

Abstract Glaucoma is a neurodegenerative disease characterized by loss of retinal ganglion cells (RGCs), the output neurons of the retina. Multiple lines of evidence show the endothelin (EDN, also known as ET) system is important in glaucomatous neurodegeneration. To date, the molecular mechanisms within RGCs driving EDN-induced RGC death have not been clarified. The pro-apoptotic transcription factor JUN (the canonical target of JNK signaling) and the endoplasmic reticulum stress effector and transcription factor DNA damage inducible transcript 3 (DDIT3, also known as CHOP) have been shown to act downstream of EDN receptors. Previous studies demonstrated that JUN and DDIT3 were important regulators of RGC death after glaucoma-relevant injures. Here, we characterized EDN insult in vivo and investigated the role of JUN and DDIT3 in EDN-induced RGC death. To accomplish this, EDN1 ligand was intravitreally injected into the eyes of wildtype, Six3-cre+Junfl/fl (Jun−/−), Ddit3 null (Ddit3−/−), and Ddit3−/−Jun−/− mice. Intravitreal EDN1 was sufficient to drive RGC death in vivo. EDN1 insult caused JUN activation in RGCs, and deletion of Jun from the neural retina attenuated RGC death after EDN insult. However, deletion of Ddit3 did not confer significant protection to RGCs after EDN1 insult. These results indicate that EDN caused RGC death via a JUN-dependent mechanism. In addition, EDN signaling is known to elicit potent vasoconstriction. JUN signaling was shown to drive neuronal death after ischemic insult. Therefore, the effects of intravitreal EDN1 on retinal vessel diameter and hypoxia were explored. Intravitreal EDN1 caused transient retinal vasoconstriction and regions of RGC and Müller glia hypoxia. Thus, it remains a possibility that EDN elicits a hypoxic insult to RGCs, causing apoptosis via JNK-JUN signaling. The importance of EDN-induced vasoconstriction and hypoxia in causing RGC death after EDN insult and in models of glaucoma requires further investigation.

Expression of the BDNF gene in the developing visual system of the chick

Development ◽  
1994 ◽  
Vol 120 (6) ◽  
pp. 1643-1649 ◽  
Author(s):  
K.H. Herzog ◽  
K. Bailey ◽  
Y.A. Barde
Keyword(s):  
Visual System ◽  
Ganglion Cells ◽  
Mrna Levels ◽  
Retinal Ganglion ◽  
Bdnf Gene ◽  
Bdnf Mrna ◽  
Optic Stalk ◽  
Copy Numbers ◽  
Activity Dependent

Using a sensitive and quantitative method, the mRNA levels of brain-derived neurotrophic factor (BDNF) were determined during the development of the chick visual system. Low copy numbers were detected, and BDNF was found to be expressed in the optic tectum already 2 days before the arrival of the first retinal ganglion cell axons, suggesting an early role of BDNF in tectal development. After the beginning of tectal innervation, BDNF mRNA levels markedly increased, and optic stalk transection at day 4 (which prevents subsequent tectal innervation) was found to reduce the contralateral tectal levels of BDNF mRNA. Comparable reductions were obtained after injection of tetrodotoxin into one eye, indicating that, already during the earliest stages of target encounter in the CNS, the degree of BDNF gene expression is influenced by activity-dependent mechanisms. BDNF mRNA was also detected in the retina itself and at levels comparable to those found in the tectum. Together with previous findings indicating that BDNF prevents the death of cultured chick retinal ganglion cells, these results support the idea that the tightly controlled expression of the BDNF gene might be important in the co-ordinated development of the visual system.

scholarly journals The Role of N-Methyl-D-Aspartate Receptor Activation in Homocysteine-Induced Death of Retinal Ganglion Cells

2011 ◽  
Vol 52 (8) ◽  
pp. 5515 ◽  
Author(s):  
Preethi S. Ganapathy ◽  
Richard E. White ◽  
Yonju Ha ◽  
B. Renee Bozard ◽  
Paul L. McNeil ◽  
...  
Keyword(s):  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Receptor Activation ◽  
Retinal Ganglion ◽  
Aspartate Receptor

scholarly journals Nav1.6 promotes inflammation and neuronal degeneration in a mouse model of multiple sclerosis

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Barakat Alrashdi ◽  
Bassel Dawod ◽  
Andrea Schampel ◽  
Sabine Tacke ◽  
Stefanie Kuerten ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Retinal Ganglion Cells ◽  
Axonal Degeneration ◽  
Ganglion Cells ◽  
Neuronal Degeneration ◽  
Retinal Ganglion ◽  
Autoimmune Encephalomyelitis ◽  
Aav Vector ◽  
Α Subunit

Abstract Background In multiple sclerosis (MS) and in the experimental autoimmune encephalomyelitis (EAE) model of MS, the Nav1.6 voltage-gated sodium (Nav) channel isoform has been implicated as a primary contributor to axonal degeneration. Following demyelination Nav1.6, which is normally co-localized with the Na+/Ca2+ exchanger (NCX) at the nodes of Ranvier, associates with β-APP, a marker of neural injury. The persistent influx of sodium through Nav1.6 is believed to reverse the function of NCX, resulting in an increased influx of damaging Ca2+ ions. However, direct evidence for the role of Nav1.6 in axonal degeneration is lacking. Methods In mice floxed for Scn8a, the gene that encodes the α subunit of Nav1.6, subjected to EAE we examined the effect of eliminating Nav1.6 from retinal ganglion cells (RGC) in one eye using an AAV vector harboring Cre and GFP, while using the contralateral either injected with AAV vector harboring GFP alone or non-targeted eye as control. Results In retinas, the expression of Rbpms, a marker for retinal ganglion cells, was found to be inversely correlated to the expression of Scn8a. Furthermore, the gene expression of the pro-inflammatory cytokines Il6 (IL-6) and Ifng (IFN-γ), and of the reactive gliosis marker Gfap (GFAP) were found to be reduced in targeted retinas. Optic nerves from targeted eyes were shown to have reduced macrophage infiltration and improved axonal health. Conclusion Taken together, our results are consistent with Nav1.6 promoting inflammation and contributing to axonal degeneration following demyelination.

scholarly journals Hyperhomocysteinemia-induced death of retinal ganglion cells: The role of Müller glial cells and NRF2

Redox Biology ◽  
2019 ◽  
Vol 24 ◽  
pp. 101199 ◽  
Author(s):  
Soumya Navneet ◽  
Jing Zhao ◽  
Jing Wang ◽  
Barbara Mysona ◽  
Shannon Barwick ◽  
...  
Keyword(s):  
Retinal Ganglion Cells ◽  
Glial Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Müller Glial Cells

scholarly journals Inhibition of microRNA-155 Protects Retinal Function Through Attenuation of Inflammation in Retinal Degeneration

2020 ◽  
Author(s):  
Riemke Aggio-Bruce ◽  
Joshua A. Chu-Tan ◽  
Yvette Wooff ◽  
Adrian V. Cioanca ◽  
Ulrike Schumann ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Retinal Degeneration ◽  
Ganglion Cells ◽  
Retinal Function ◽  
Retinal Ganglion ◽  
Retinal Tissue ◽  
Inflammatory Conditions ◽  
Retinal Degenerative Diseases ◽  
Negative Controls

Abstract Although extensively investigated in inflammatory conditions, the role of pro-inflammatory microRNAs (miRNAs), miR-155 and miR-146a, has not been well-studied in retinal degenerative diseases. We therefore aimed to explore the role and regulation of these miRNA in the degenerating retina, with a focus on miR-155. C57BL/6J mice were subjected to photo-oxidative damage for up to 5 days to induce focal retinal degeneration. MiR-155 expression was quantified by qRT-PCR in whole retina, serum, and small-medium extracellular vesicles (s-mEVs), and a PrimeFlow™ assay was used to identify localisation of miR-155 in retinal cells. Constitutive miR-155 knockout (KO) mice and miR-155 and miR-146a inhibitors were utilised to determine the role of these miRNA in the degenerating retina. Electroretinography was employed as a measure of retinal function, while histological quantification of TUNEL+ and IBA1+ positive cells was used to quantify photoreceptor cell death and infiltrating immune cells, respectively. Upregulation of miR-155 was detected in retinal tissue, serum and s-mEVs in response to photo-oxidative damage, localising to the nucleus of a subset of retinal ganglion cells and glial cells and in the cytoplasm of photoreceptors. Inhibition of miR-155 showed increased function from negative controls and a less pathological pattern of IBA1+ cell localisation and morphology at 5 days photo-oxidative damage. While neither dim-reared nor damaged miR-155 KO animals showed retinal histological difference from controls, following photo-oxidative damage, miR-155 KO mice showed increased a-wave relative to controls. We therefore consider miR-155 to be associated with the inflammatory response of the retina in response to photoreceptor-specific degeneration.

Role of Eye Movements in the Retinal Code for a Size Discrimination Task

2007 ◽  
Vol 98 (3) ◽  
pp. 1380-1391 ◽  
Author(s):  
Ronen Segev ◽  
Elad Schneidman ◽  
Joe Goodhouse ◽  
Michael J. Berry
Keyword(s):  
Eye Movements ◽  
Visual Information ◽  
Ganglion Cells ◽  
Multielectrode Array ◽  
Retinal Ganglion ◽  
Size Discrimination ◽  
Fixational Eye Movements ◽  
Stationary Objects ◽  
A Minor

The concerted action of saccades and fixational eye movements are crucial for seeing stationary objects in the visual world. We studied how these eye movements contribute to retinal coding of visual information using the archer fish as a model system. We quantified the animal's ability to distinguish among objects of different sizes and measured its eye movements. We recorded from populations of retinal ganglion cells with a multielectrode array, while presenting visual stimuli matched to the behavioral task. We found that the beginning of fixation, namely the time immediately after the saccade, provided the most visual information about object size, with fixational eye movements, which consist of tremor and drift in the archer fish, yielding only a minor contribution. A simple decoder that combined information from ≤15 ganglion cells could account for the behavior. Our results support the view that saccades impose not just difficulties for the visual system, but also an opportunity for the retina to encode high quality “snapshots” of the environment.

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