The Inflation Response of Mouse Sclera: Age Effects on the Mechanical Properties of Scleral Tissue

2010 ◽  
Author(s):  
Kristin M. Myers ◽  
Frances Cone ◽  
Harry Quigley ◽  
Baptiste Coudrillier ◽  
Thao D. Nguyen
Keyword(s):  
Material Properties ◽  
Visual Information ◽  
Vision Loss ◽  
Ganglion Cells ◽  
The United States ◽  
Ocular Tissue ◽  
Mouse Strains ◽  
Retinal Ganglion ◽  
Deformation Response

The mouse model offers an opportunity to investigate how alterations to the connective soft tissue contribute to the development of disease through the study of transgenic and diseased mouse strains. For example, by measuring the deformation response of the eye wall to increases in pressure of these different mouse types, the possible role of ocular tissue material properties in glaucomatous damage can be determined. Glaucoma is one of the leading causes of blindness in the United States and in the world with an estimate of 60 million people affected by this year [1]. It is caused by damage to the retinal ganglion cells (RGC), a type of neuron that transmits visual information to the brain. Despite therapeutic efforts to reduce the rate of vision loss in glaucoma patients, the rate of blindness remains high [2]. There is evidence that elevated intraocular pressure (IOP) is a strong risk factor for the disease [3–5], and it is hypothesized that possible alterations in the time-dependent scleral material properties may play an important role in cumulative RGC death.

The Bulge Inflation Response of Bovine Sclera

2009 ◽  
Author(s):  
Kristin M. Myers ◽  
Thao D. Nguyen
Keyword(s):  
Visual Information ◽  
Vision Loss ◽  
Mechanical Response ◽  
Ganglion Cells ◽  
The United States ◽  
Retinal Ganglion ◽  
Tissue Samples ◽  
Strip Testing ◽  
The Relationship ◽  
The Brain

Glaucoma is one of the leading causes of blindness in the United States and in the world [1]. It is caused by damage to the retinal ganglion cells (RGC), a type of neuron that transmits visual information to the brain. Despite therapeutic efforts to reduce the rate of vision loss in glaucoma patients, the rate of blindness remains high [2]. There is evidence that elevated intraocular pressure (IOP) plays an important role in the damage to RGCs [3–5], but the relationship between the mechanical properties of the connective tissue and how it affects the cellular function is not understood. The load-bearing eye wall consists of the cornea and the sclera. Both tissues are collagen rich structures with preferentially aligned collagen lamellae dictating its mechanical response. Previous studies have shown that the viscoelastic material response of the eye wall differs between normal and glaucoma animal tissues [6]. However, these previous studies relied on strip testing of tissue samples.

Modeling the Inflation Response of C57BL/6 Mouse Sclera

2011 ◽  
Author(s):  
Kristin M. Myers ◽  
Thao D. Nguyen
Keyword(s):  
Material Properties ◽  
Soft Tissues ◽  
Ganglion Cells ◽  
The United States ◽  
Small Rodent ◽  
Tissue Samples ◽  
Tissue Microstructure ◽  
Material Parameters ◽  
Meaningful Material

Small rodent models have become increasingly useful to investigate how the mechanical properties of soft tissues may influence disease development. These animal models allow access to aged, diseased, or genetically-altered tissue samples, and through comparisons with wild-type or normal tissue it can be explored how each of these variables influence tissue function. The challenges to deriving meaningful material parameters for these small tissue samples include designing physiologically-relevant mechanical testing protocols and interpreting the experimental load-displacement data in an appropriate constitutive framework to quantify material parameters. This study was motivated by determining the possible role of scleral material properties in the development of glaucomatous damage to the retinal ganglion cells (RGC). Glaucoma is one of the leading causes of blindness in the United States and in the world with an estimate of 60 million people affected by this year [1]. Through exploring mouse models, the overall goal of our work is to determine the role of scleral material properties and scleral tissue microstructure in the pathogenesis of glaucoma.

The Biomechanical Response of Normal and Glaucoma Human Sclera

2010 ◽  
Author(s):  
Baptiste Coudrillier ◽  
Kristin M. Myers ◽  
Thao D. Nguyen
Keyword(s):  
Retinal Ganglion Cells ◽  
Material Properties ◽  
Visual Information ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Progressive Degeneration ◽  
Biomechanical Response ◽  
Elevated Intraocular Pressure ◽  
The Relationship ◽  
The Brain

By 2010, 60 million people will have glaucoma, the second leading cause of blindness worldwide [1]. The disease is characterized by a progressive degeneration of the retinal ganglion cells (RGC), a type of neuron that transmits visual information to the brain. It is well know that elevated intraocular pressure (IOP) is a risk factor in the damage to the RGCs [3–5], but the relationship between the mechanical properties of the ocular connective tissue and how it affects cellular function is not well characterized. The cornea and the sclera are collage-rich structures that comprise the outer load-bearing shell of the eye. Their preferentially aligned collagen lamellae provide mechanical strength to resist ocular expansion. Previous uniaxial tension studies suggest that altered viscoelastic material properties of the eye wall play a role in glaucomatous damage [6].

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.

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.

scholarly journals Neuroprotective Role of GLP-1 Analog for Retinal Ganglion Cells via PINK1/Parkin-Mediated Mitophagy in Diabetic Retinopathy

2021 ◽  
Vol 11 ◽  
Author(s):  
Huan-ran Zhou ◽  
Xue-fei Ma ◽  
Wen-jian Lin ◽  
Ming Hao ◽  
Xin-yang Yu ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Retinal Ganglion Cells ◽  
Visual Information ◽  
Ganglion Cells ◽  
Neuroprotective Effect ◽  
Diabetic Rat ◽  
Retinal Ganglion

GLP-1 analogs have been widely used to treat patients with type 2 diabetes in recent years and studies have found that GLP-1 analogs have multiple organ benefits. However, the role of GLP-1 analogs in diabetic retinopathy (DR), a common complication of diabetes mellitus (DM), remains controversial. Retinal ganglion cells (RGCs) are the only afferent neurons responsible for transmitting visual information to the visual center and are vulnerable in the early stage of DR. Protection of RGC is vital for visual function. The incretin glucagon-like peptide-1 (GLP-1), which is secreted by L-cells after food ingestion, could lower blood glucose level through stimulating the release of insulin. In the present study, we evaluated the effects of GLP-1 analog on RGCs both in vitro and in vivo. We established diabetic rat models in vivo and applied an RGC-5 cell line in vitro. The results showed that in high glucose conditions, GLP-1 analog alleviated the damage of RGCs. In addition, GLP-1 analog prevented mitophagy through the PINK1/Parkin pathway. Here we demonstrated the neuroprotective effect of GLP-1 analog, which may be beneficial for retinal function, and we further elucidated a novel mechanism in GLP-1 analog-regulated protection of the retina. These findings may expand the multi-organ benefits of GLP-1 analogs and provide new insights for the prevention of DR.

Glaucoma management in the era of artificial intelligence

2019 ◽  
Vol 104 (3) ◽  
pp. 301-311 ◽  
Author(s):  
Sripad Krishna Devalla ◽  
Zhang Liang ◽  
Tan Hung Pham ◽  
Craig Boote ◽  
Nicholas G Strouthidis ◽  
...  
Keyword(s):  
Artificial Intelligence ◽  
Deep Learning ◽  
Retinal Ganglion Cells ◽  
Vision Loss ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Irreversible Damage ◽  
Diagnosis And Prognosis ◽  
Disease Prognosis

Glaucoma is a result of irreversible damage to the retinal ganglion cells. While an early intervention could minimise the risk of vision loss in glaucoma, its asymptomatic nature makes it difficult to diagnose until a late stage. The diagnosis of glaucoma is a complicated and expensive effort that is heavily dependent on the experience and expertise of a clinician. The application of artificial intelligence (AI) algorithms in ophthalmology has improved our understanding of many retinal, macular, choroidal and corneal pathologies. With the advent of deep learning, a number of tools for the classification, segmentation and enhancement of ocular images have been developed. Over the years, several AI techniques have been proposed to help detect glaucoma by analysis of functional and/or structural evaluations of the eye. Moreover, the use of AI has also been explored to improve the reliability of ascribing disease prognosis. This review summarises the role of AI in the diagnosis and prognosis of glaucoma, discusses the advantages and challenges of using AI systems in clinics and predicts likely areas of future progress.

scholarly journals Regeneration of Functional Retinal Ganglion Cells by Neuronal Identity Reprogramming

2020 ◽  
Author(s):  
Xiaohu Wei ◽  
Zhenhao Zhang ◽  
Huan-huan Zeng ◽  
Xue-Feng Wang ◽  
Wenrong Zhan ◽  
...  
Keyword(s):  
Retinal Ganglion Cells ◽  
Visual Information ◽  
Therapeutic Strategy ◽  
Vision Loss ◽  
Visual Stimulation ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Adult Mice ◽  
Lineage Reprogramming ◽  
The Brain

SUMMARYDegeneration of retinal ganglion cells (RGCs) and their axons underlies vision loss in glaucoma and various optic neuropathies. There are currently no treatments available to restore lost vision in patients affected by these diseases. Regenerating RGCs and reconnecting the retina to the brain represent an ideal therapeutic strategy; however, mammals do not have a reservoir of retinal stem/progenitor cells poised to produce new neurons in adulthood. Here, we regenerated RGCs in adult mice by direct lineage reprogramming of retinal interneurons. We successfully converted amacrine and displaced amacrine interneurons into RGCs, and observed that regenerated RGCs projected axons into brain retinorecipient areas. They convey visual information to the brain in response to visual stimulation, and are able to transmit electrical signals to postsynaptic neurons, in both normal animals and in a diseased model. The generation of functional RGCs in adult mammals points to a therapeutic strategy for vision restoration in patients.

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.

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