Biomechanics of the Posterior Pole During the Remodeling Progression From Normal to Early Experimental Glaucoma

2009 ◽  
Author(s):  
Ian A. Sigal ◽  
Hongli Yang ◽  
Michael D. Roberts ◽  
Claude F. Burgoyne ◽  
J. Crawford Downs
Keyword(s):  
Visual Information ◽  
Lamina Cribrosa ◽  
Posterior Pole ◽  
Glaucomatous Optic Neuropathy ◽  
Retinal Ganglion ◽  
Experimental Glaucoma ◽  
Pass Through ◽  
Mechanical Insult ◽  
The Brain ◽  
Connective Tissue Structure

Glaucoma is one of the leading causes of blindness worldwide. The loss of vision associated with glaucoma is due to damage to the retinal ganglion cell axons, which transmit visual information to the brain. Damage to these axons is believed to occur as the axons pass through the lamina cribrosa (LC), a connective tissue structure in the optic nerve head at the back of the eye. Elevated intraocular pressure (IOP) has been identified as the main risk factor for the development of the neuropathy, but the mechanism(s) by which a mechanical insult (elevated IOP) is translated into a biological effect (glaucomatous optic neuropathy) is not well understood.

Microstructure Motivated Growth and Remodeling of the Lamina Cribrosa in Early Glaucoma

2011 ◽  
Author(s):  
Rafael Grytz ◽  
Ian A. Sigal ◽  
Jeffrey W. Ruberti ◽  
J. Crawford Downs
Keyword(s):  
Connective Tissue ◽  
Structural Changes ◽  
Lamina Cribrosa ◽  
Posterior Pole ◽  
Retinal Ganglion ◽  
Experimental Glaucoma ◽  
Relevant Risk Factor ◽  
Orbital Space ◽  
Iop Elevation ◽  
Pass Through

Glaucoma is a leading cause of blindness in the world and is due to the loss of retinal ganglion cell axons. These axons deteriorate in a region in the posterior pole of the eye known as the optic nerve head (ONH). The axons pass through the lamina cribrosa (LC) as they exit the eye at the ONH. The LC is characterized by a porous, connective tissue structure composed of laminar beams. The function of the LC is unclear, but is believed to include providing mechanical support to the axons as they transition from inside the pressurized globe to the lower pressure orbital space. Early experimental glaucoma studies have shown that the LC remodels into a thicker, more posterior structure which incorporates more connective tissue after chronic IOP elevation [1,2]. The process by which this occurs is unknown. These structural changes are assumed to play an important role in the pathophysiology of the ocular disease glaucoma, where elevated IOP is known to be the most relevant risk factor.

Finite Element Modeling of the Lamina Cribrosa Microarchitecture in the Normal and Early Glaucoma Monkey Optic Nerve Head

2007 ◽  
Author(s):  
J. Crawford Downs ◽  
Michael D. Roberts ◽  
Claude F. Burgoyne ◽  
Richard T. Hart
Keyword(s):  
Optic Nerve ◽  
Optic Nerve Head ◽  
Nutritional Support ◽  
Lamina Cribrosa ◽  
Retinal Ganglion ◽  
The Us ◽  
Elevated Intraocular Pressure ◽  
Pass Through ◽  
The Brain ◽  
Connective Tissue Structure

Glaucoma is the second leading cause of blindness in the US and is usually associated with elevated intraocular pressure (IOP). Glaucomatous damage is believed to occur at the optic nerve head (ONH) where the retinal ganglion cell axons pass through an opening in the back of the eye wall on their path to the brain. This opening is spanned by the lamina cribrosa, a fenestrated connective tissue structure that provides structural and nutritional support for the axons as they pass through the eye wall.

Next-Generation Techniques for Analysis of Lamina Cribrosa Microstructure

2012 ◽  
Author(s):  
C. Ross Ethier ◽  
Richie Abel ◽  
E. A. Sander ◽  
John G. Flanagan ◽  
Michael Girard
Keyword(s):  
Risk Factor ◽  
Intraocular Pressure ◽  
Retinal Ganglion Cells ◽  
Visual Information ◽  
Ganglion Cells ◽  
Lamina Cribrosa ◽  
Retinal Ganglion ◽  
Irreversible Damage ◽  
Ocular Disorders ◽  
The Brain

Glaucoma describes a group of potentially blinding ocular disorders, afflicting c. 60 million people worldwide. Of these, c. 8 million are bilaterally blind, estimated to increase to 11 million by 2020. The central event in glaucoma is slow and irreversible damage of retinal ganglion cells, responsible for carrying visual information from the retina to the brain (Figure 1). Intraocular pressure (IOP) is a risk factor for glaucoma1–4, and significant, sustained IOP reduction is unequivocally beneficial in the clinical management of glaucoma patients2, 3, 5. Unfortunately, we do not understand how elevated IOP leads to the loss of retinal ganglion cells.

Analysis of Experimental IOP-Induced Scleral Deformations at the Sub-Micrometer Scale Using Electronic Speckle Interferometry

2011 ◽  
Author(s):  
Massimo A. Fazio ◽  
Luigi Bruno ◽  
Rafael Grytz ◽  
J. Crawford Downs
Keyword(s):  
Visual Information ◽  
Computational Models ◽  
Speckle Interferometry ◽  
Posterior Pole ◽  
Retinal Ganglion ◽  
Electronic Speckle Interferometry ◽  
Ocular Biomechanics ◽  
Pass Through ◽  
Scleral Shell ◽  
Micrometer Scale

The retinal ganglion cell axons carry visual information, and pass through the optic nerve head (ONH) as they traverse from inside the eye to the brain. The ONH is the site of axonal damage in glaucoma, the second leading cause of blindness in the world, and ONH biomechanics is hypothesized to play a crucial role in the development and progression of the disease. The load bearing tissues of the ONH insert into the surrounding sclera, which provides the boundary conditions for this important structure. It is therefore important to develop accurate experimental techniques to measure scleral shell deformations under intraocular pressure (IOP) loading that can be used to drive constitutive and computational models of scleral biomechanics. The overall goal of this project is to better understand the role of ocular biomechanics in the development of glaucoma by constructing eye-specific finite element models of the posterior pole and ONH.

Continuum-Level Finite Element Modeling of the Optic Nerve Head Using a Fabric Tensor Based Description of the Lamina Cribrosa

2007 ◽  
Author(s):  
Michael D. Roberts ◽  
Richard T. Hart ◽  
Yi Liang ◽  
Anthony J. Bellezza ◽  
Claude F. Burgoyne ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Optic Nerve Head ◽  
Ganglion Cells ◽  
Lamina Cribrosa ◽  
Vision Impairment ◽  
Porous Space ◽  
Fabric Tensor ◽  
Retinal Ganglion ◽  
Pass Through ◽  
Connective Tissue Structure

Glaucoma is a chronic disease of the eye that can progress to severe vision impairment or blindness if left untreated. The principal site of glaucomatous damage is believed to be within the optic nerve head (ONH) where the axons of the retinal ganglion cells pass through an opening in the back of the sclera (the eye wall) on their way to form the orbital optic nerve. This opening is spanned by the lamina cribrosa (LC), a fenestrated connective tissue structure which provides both a load bearing function for the eye as well as support (both structural and metabolic) for axonal bundles as they traverse the porous space of the LC.

scholarly journals A method for single-neuron chronic recording from the retina in awake mice

Science ◽  
2018 ◽  
Vol 360 (6396) ◽  
pp. 1447-1451 ◽  
Author(s):  
Guosong Hong ◽  
Tian-Ming Fu ◽  
Mu Qiao ◽  
Robert D. Viveros ◽  
Xiao Yang ◽  
...  
Keyword(s):  
Retinal Ganglion Cells ◽  
Visual Information ◽  
Single Neuron ◽  
Ganglion Cells ◽  
Ex Vivo ◽  
Neural Circuitry ◽  
Retinal Ganglion ◽  
Chronic Recording ◽  
The Brain

The retina, which processes visual information and sends it to the brain, is an excellent model for studying neural circuitry. It has been probed extensively ex vivo but has been refractory to chronic in vivo electrophysiology. We report a nonsurgical method to achieve chronically stable in vivo recordings from single retinal ganglion cells (RGCs) in awake mice. We developed a noncoaxial intravitreal injection scheme in which injected mesh electronics unrolls inside the eye and conformally coats the highly curved retina without compromising normal eye functions. The method allows 16-channel recordings from multiple types of RGCs with stable responses to visual stimuli for at least 2 weeks, and reveals circadian rhythms in RGC responses over multiple day/night cycles.

Age-Related Changes in Scleral Material Properties of the Monkey Eye

2008 ◽  
Author(s):  
Michaël J. A. Girard ◽  
Jun-Kyo F. Suh ◽  
Michael Bottlang ◽  
Claude F. Burgoyne ◽  
J. Crawford Downs
Keyword(s):  
Intraocular Pressure ◽  
Material Properties ◽  
Lamina Cribrosa ◽  
Collagen Fibers ◽  
Visual Signals ◽  
Type I ◽  
Retinal Ganglion ◽  
Age Related ◽  
The Brain ◽  
Age Related Changes

The sclera is the outer shell and principal load-bearing tissue of the eye, which consists primarily of avascular lamellae of collagen fibers. Ninety percent of the collagen fibers in the sclera are Type I, which provide the eye with necessary mechanical strength to sustain intraocular pressure (IOP). In the posterior sclera, there is a fenestrated canal, called the optic nerve head (ONH), through which the retinal ganglion cell axons pass transmitting visual signals from the retina to the brain. The opening of the ONH is structurally supported by a fenestrated connective tissue called the lamina cribrosa.

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].

scholarly journals Molecular codes for cell type specification in Brn3 retinal ganglion cells

2017 ◽  
Vol 114 (20) ◽  
pp. E3974-E3983 ◽  
Author(s):  
Szilard Sajgo ◽  
Miruna Georgiana Ghinia ◽  
Matthew Brooks ◽  
Friedrich Kretschmer ◽  
Katherine Chuang ◽  
...  
Keyword(s):  
Retinal Ganglion Cells ◽  
Visual Information ◽  
Ganglion Cells ◽  
Neuronal Cell ◽  
Neuronal Morphology ◽  
Retinal Ganglion ◽  
Cell Type ◽  
Type Specification ◽  
The Brain ◽  
Combinatorial Code

Visual information is conveyed from the eye to the brain by distinct types of retinal ganglion cells (RGCs). It is largely unknown how RGCs acquire their defining morphological and physiological features and connect to upstream and downstream synaptic partners. The three Brn3/Pou4f transcription factors (TFs) participate in a combinatorial code for RGC type specification, but their exact molecular roles are still unclear. We use deep sequencing to define (i) transcriptomes of Brn3a- and/or Brn3b-positive RGCs, (ii) Brn3a- and/or Brn3b-dependent RGC transcripts, and (iii) transcriptomes of retinorecipient areas of the brain at developmental stages relevant for axon guidance, dendrite formation, and synaptogenesis. We reveal a combinatorial code of TFs, cell surface molecules, and determinants of neuronal morphology that is differentially expressed in specific RGC populations and selectively regulated by Brn3a and/or Brn3b. This comprehensive molecular code provides a basis for understanding neuronal cell type specification in RGCs.

scholarly journals Effects of Iron and Zinc on Mitochondria: Potential Mechanisms of Glaucomatous Injury

2021 ◽  
Vol 9 ◽  
Author(s):  
Jiahui Tang ◽  
Yehong Zhuo ◽  
Yiqing Li
Keyword(s):  
Ganglion Cell ◽  
Retinal Ganglion Cells ◽  
Visual Information ◽  
Ganglion Cells ◽  
Cell Damage ◽  
Current View ◽  
Retinal Ganglion ◽  
Mitochondrial Homeostasis ◽  
Iron And Zinc ◽  
The Brain

Glaucoma is the most substantial cause of irreversible blinding, which is accompanied by progressive retinal ganglion cell damage. Retinal ganglion cells are energy-intensive neurons that connect the brain and retina, and depend on mitochondrial homeostasis to transduce visual information through the brain. As cofactors that regulate many metabolic signals, iron and zinc have attracted increasing attention in studies on neurons and neurodegenerative diseases. Here, we summarize the research connecting iron, zinc, neuronal mitochondria, and glaucomatous injury, with the aim of updating and expanding the current view of how retinal ganglion cells degenerate in glaucoma, which can reveal novel potential targets for neuroprotection.

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