scholarly journals The Glial Design of a Teleost Optic Nerve Head Supporting Continuous Growth

2002 ◽  
Vol 50 (10) ◽  
pp. 1289-1302 ◽  
Author(s):  
Concepción Lillo ◽  
Almudena Velasco ◽  
David Jimeno ◽  
Elena Cid ◽  
Juan M. Lara ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Optic Nerve Head ◽  
Ganglion Cells ◽  
Müller Cells ◽  
Nuclear Antigen ◽  
Muller Cells ◽  
Continuous Growth ◽  
Dividing Cells ◽  
Regional Adaptation ◽  
Tench Tinca Tinca

This study demonstrates the peculiarities of the glial organization of the optic nerve head (ONH) of a fish, the tench ( Tinca tinca), by using immunohistochemistry and electron microscopy. We employed antibodies specific for the macroglial cells: glutamine synthetase (GS), glial fibrillary acidic protein (GFAP), and S100. We also used the N518 antibody to label the new ganglion cells' axons, which are continuously added to the fish retina, and the anti-proliferating cell nuclear antigen (PCNA) antibody to specifically locate dividing cells. We demonstrate a specific regional adaptation of the GS-S100-positive Müller cells' vitreal processes around the optic disc, strongly labeled with the anti-GFAP antibody. In direct contact with these Müller cells' vitreal processes, there are S100-positive astrocytes and S100-negative cells ultrastructurally identified as microglial cells. Moreover, a population of PCNA-positive cells, characterized as glioblasts, forms the limit between the retina and the optic nerve in a region homologous to the Kuhnt intermediary tissue of mammals. Finally, in the intraocular portion of the optic nerve there are differentiating oligodendrocytes arranged in rows. Both the glioblasts and the rows of developing cells could serve as a pool of glial elements for the continuous growth of the visual system.

scholarly journals Retinal Ganglion Cells Downregulate Gene Expression and Lose Their Axons within the Optic Nerve Head in a Mouse Glaucoma Model

2008 ◽  
Vol 28 (2) ◽  
pp. 548-561 ◽  
Author(s):  
I. Soto ◽  
E. Oglesby ◽  
B. P. Buckingham ◽  
J. L. Son ◽  
E. D. O. Roberson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Optic Nerve ◽  
Retinal Ganglion Cells ◽  
Optic Nerve Head ◽  
Ganglion Cells ◽  
Retinal Ganglion

scholarly journals Retinal hemorrhages as one of complications of optic disc drusen during pregnancy

2014 ◽  
Vol 67 (5-6) ◽  
pp. 185-189
Author(s):  
Marija Trenkic-Bozinovic ◽  
Predrag Jovanovic ◽  
Gordana Zlatanovic ◽  
Dragan Veselinovic ◽  
Aleksandra Aracki-Trenkic ◽  
...  
Keyword(s):  
Visual Acuity ◽  
Optic Nerve ◽  
Visual Field ◽  
Optic Disc ◽  
Optic Nerve Head ◽  
Ganglion Cells ◽  
Therapeutic Interventions ◽  
Visual Field Defects ◽  
Retinal Hemorrhages ◽  
Optic Disc Drusen

Introduction. Drusen of the optic nerve head are relatively benign and asymptomatic. They represent retinal hyaline corpuscles resulting from impaired axoplasmic transport of the retinal ganglion cells of optic nerve in front of the lamina cribrosa. They are usually detected accidentally, during a routine ophthalmologic examination. Most patients with optic disc drusen are not aware of the deterioration of their eyesight because of the slow progression of visual field defects. Damage in visual acuity due to optic disc drusen is rare. Case Report. A 27-year-old female patient in the sixth month of pregnancy visited an ophthalmologist because of a visual impairment described as the appearance of mist and shadows over her right eye. When first examined, her visual acuity in both eyes was 20/20. The retinal hemorrhages framing the bottom half of the optic nerve were seen. Complete laboratory and clinical testing as well as specific ophthalmic examinations (photofundus, computerized visual field, optical coherence tomography, and ultrasound) were performed to exclude systemic causes and they presented no risk for the pregnancy. Echosonographic examination confirmed the presence of bilateral optic nerve head drusen. Conclusion. Hemodynamic changes during pregnancy are possible factors for the development of optical disc and retinal hemorrhages. Since treatment of optic disc drusen is limited, recognition of optic nerve drusen as a cause of hemorrhage during pregnancy prevents unnecessary diagnostic and therapeutic interventions.

scholarly journals A Methodology for Individual-Specific Modeling of Rat Optic Nerve Head Biomechanics in Glaucoma

2018 ◽  
Vol 140 (8) ◽  
Author(s):  
Stephen A. Schwaner ◽  
Alison M. Kight ◽  
Robert N. Perry ◽  
Marta Pazos ◽  
Hongli Yang ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Optic Nerve Head ◽  
Cellular Response ◽  
Ganglion Cells ◽  
Axonal Injury ◽  
Retinal Ganglion ◽  
Mechanistic Studies ◽  
Specific Modeling ◽  
Initial Results ◽  
Model Strain

Glaucoma is the leading cause of irreversible blindness and involves the death of retinal ganglion cells (RGCs). Although biomechanics likely contributes to axonal injury within the optic nerve head (ONH), leading to RGC death, the pathways by which this occurs are not well understood. While rat models of glaucoma are well-suited for mechanistic studies, the anatomy of the rat ONH is different from the human, and the resulting differences in biomechanics have not been characterized. The aim of this study is to describe a methodology for building individual-specific finite element (FE) models of rat ONHs. This method was used to build three rat ONH FE models and compute the biomechanical environment within these ONHs. Initial results show that rat ONH strains are larger and more asymmetric than those seen in human ONH modeling studies. This method provides a framework for building additional models of normotensive and glaucomatous rat ONHs. Comparing model strain patterns with patterns of cellular response seen in studies using rat glaucoma models will help us to learn more about the link between biomechanics and glaucomatous cell death, which in turn may drive the development of novel therapies for glaucoma.

scholarly journals A dialogue between glia and neurons in the retina: modulation of neuronal excitability

2004 ◽  
Vol 1 (3) ◽  
pp. 245-252 ◽  
Author(s):  
ERIC A. NEWMAN
Keyword(s):  
Synaptic Transmission ◽  
Glial Cells ◽  
Neuronal Excitability ◽  
Ganglion Cells ◽  
Brain Slices ◽  
Müller Cells ◽  
Muller Cells ◽  
Signaling Mechanisms ◽  
Bidirectional Signaling ◽  
Stimulation Of

Bidirectional signaling between neurons and glial cells has been demonstrated in brain slices and is believed to mediate glial modulation of synaptic transmission in the CNS. Our laboratory has characterized similar neuron–glia signaling in the mammalian retina. We find that light-evoked neuronal activity elicits Ca2+ increases in Müller cells, which are specialized retinal glial cells. Neuron to glia signaling is likely mediated by the release of ATP from neurons and is potentiated by adenosine. Glia to neuron signaling has also been observed and is mediated by several mechanisms. Stimulation of glial cells can result in either facilitation or depression of synaptic transmission. Release of D-serine from Müller cells might also potentiate NMDA receptor transmission. Müller cells directly inhibit ganglion cells by releasing ATP, which, following hydrolysis to adenosine, activates neuronal A1 receptors. The existence of bidirectional signaling mechanisms indicates that glial cells participate in information processing in the retina.

scholarly journals An Overview of Glaucoma: Bidirectional Translation between Humans and Pre-Clinical Animal Models

2021 ◽  
Author(s):  
Sophie Pilkinton ◽  
T.J. Hollingsworth ◽  
Brian Jerkins ◽  
Monica M. Jablonski
Keyword(s):  
Risk Factor ◽  
Intraocular Pressure ◽  
Optic Nerve ◽  
Animal Models ◽  
Retinal Ganglion Cells ◽  
Optic Nerve Head ◽  
Ganglion Cells ◽  
Treatment Modalities ◽  
Retinal Ganglion ◽  
Glaucomatous Damage

Glaucoma is a multifactorial, polygenetic disease with a shared outcome of loss of retinal ganglion cells and their axons, which ultimately results in blindness. The most common risk factor of this disease is elevated intraocular pressure (IOP), although many glaucoma patients have IOPs within the normal physiological range. Throughout disease progression, glial cells in the optic nerve head respond to glaucomatous changes, resulting in glial scar formation as a reaction to injury. This chapter overviews glaucoma as it affects humans and the quest to generate animal models of glaucoma so that we can better understand the pathophysiology of this disease and develop targeted therapies to slow or reverse glaucomatous damage. This chapter then reviews treatment modalities of glaucoma. Revealed herein is the lack of non-IOP-related modalities in the treatment of glaucoma. This finding supports the use of animal models in understanding the development of glaucoma pathophysiology and treatments.

Interactions Between Factors Influencing Optic Nerve Head Biomechanics

2007 ◽  
Author(s):  
Ian A. Sigal ◽  
John G. Flanagan ◽  
C. Ross Ethier
Keyword(s):  
Optic Nerve ◽  
Optic Nerve Head ◽  
Mechanical Response ◽  
Ganglion Cells ◽  
Cell Damage ◽  
Mechanical Strain ◽  
Lamina Cribrosa ◽  
Retinal Ganglion ◽  
The Finite Element Method ◽  
Primary Risk Factor

Glaucoma is the second most common cause of blindness worldwide, and elevated intraocular pressure (IOP) is the primary risk factor for developing this disease. It has been postulated that IOP-induced mechanical strain on optic nerve head (ONH) glial cells leads to retinal ganglion cell damage and the consequent loss of vision in glaucoma. To better evaluate this theory it is important to understand the biomechanical environment within the ONH. Unfortunately it is very difficult to make measurements in the ONH, and it is particularly difficult to access the region in the ONH where the ganglion cells are thought to be injured, namely the lamina cribrosa. We have therefore developed models of the ONH and used the finite element method (FEM) to predict ONH mechanical response to changes in IOP [1].

scholarly journals Effects of Adult Müller Cells and Their Conditioned Media on the Survival of Stem Cell-Derived Retinal Ganglion Cells

Cells ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 1759
Author(s):  
Xandra Pereiro ◽  
Adam M. Miltner ◽  
Anna La Torre ◽  
Elena Vecino
Keyword(s):  
Stem Cell ◽  
Cell Survival ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Müller Cells ◽  
Cell Types ◽  
Conditioned Media ◽  
Retinal Ganglion ◽  
Muller Cells ◽  
Müller Glia

Retinal neurons, particularly retinal ganglion cells (RGCs), are susceptible to the degenerative damage caused by different inherited conditions and environmental insults, leading to irreversible vision loss and, ultimately, blindness. Numerous strategies are being tested in different models of degeneration to restore vision and, in recent years, stem cell technologies have offered novel avenues to obtain donor cells for replacement therapies. To date, stem cell–based transplantation in the retina has been attempted as treatment for photoreceptor degeneration, but the same tools could potentially be applied to other retinal cell types, including RGCs. However, RGC-like cells are not an abundant cell type in stem cell–derived cultures and, often, these cells degenerate over time in vitro. To overcome this limitation, we have taken advantage of the neuroprotective properties of Müller glia (one of the main glial cell types in the retina) and we have examined whether Müller glia and the factors they secrete could promote RGC-like cell survival in organoid cultures. Accordingly, stem cell-derived RGC-like cells were co-cultured with adult Müller cells or Müller cell-conditioned media was added to the cultures. Remarkably, RGC-like cell survival was substantially enhanced in both culture conditions, and we also observed a significant increase in their neurite length. Interestingly, Atoh7, a transcription factor required for RGC development, was up-regulated in stem cell-derived organoids exposed to conditioned media, suggesting that Müller cells may also enhance the survival of retinal progenitors and/or postmitotic precursor cells. In conclusion, Müller cells and the factors they release promote organoid-derived RGC-like cell survival, neuritogenesis, and possibly neuronal maturation.

scholarly journals Creatine transporter localization in developing and adult retina: importance of creatine to retinal function

2005 ◽  
Vol 289 (4) ◽  
pp. C1015-C1023 ◽  
Author(s):  
Monica L. Acosta ◽  
Michael Kalloniatis ◽  
David L. Christie
Keyword(s):  
Ganglion Cells ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Müller Cells ◽  
Nerve Fibers ◽  
Retinal Function ◽  
Mouse Retina ◽  
Muller Cells ◽  
Creatine Transporter ◽  
Subsequent Decrease

Creatine and phosphocreatine are required to maintain ATP needed for normal retinal function and development. The aim of the present study was to determine the distribution of the creatine transporter (CRT) to gain insight to how creatine is transported into the retina. An affinity-purified antibody raised against the CRT was applied to adult vertebrate retinas and to mouse retina during development. Confocal microscopy was used to identify the localization pattern as well as co-localization patterns with a range of retinal neurochemical markers. Strong labeling of the CRT was seen in the photoreceptor inner segments in all species studied and labeling of a variety of inner neuronal cells (amacrine, bipolar, and ganglion cells), the retinal nerve fibers and sites of creatine transport into the retina (retinal pigment epithelium, inner retinal blood vessels, and perivascular astrocytes). The CRT was not expressed in Müller cells of any of the species studied. The lack of labeling of Müller cells suggests that neurons are independent of this glial cell in accumulating creatine. During mouse retinal development, expression of the CRT progressively increased throughout the retina until approximately postnatal day 10, with a subsequent decrease. Comparison of the distribution patterns of the CRT in vascular and avascular vertebrate retinas and studies of the mouse retina during development indicate that creatine and phosphocreatine are important for ATP homeostasis.

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