scholarly journals Apolipoprotein E Is Synthesized in the Retina by Müller Glial Cells, Secreted into the Vitreous, and Rapidly Transported into the Optic Nerve by Retinal Ganglion Cells

1996 ◽  
Vol 271 (10) ◽  
pp. 5628-5632 ◽  
Author(s):  
Anil Amaratunga ◽  
Carmela R. Abraham ◽  
Ross B. Edwards ◽  
Julie H. Sandell ◽  
Barbara M. Schreiber ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Apolipoprotein E ◽  
Retinal Ganglion Cells ◽  
Glial Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Müller Glial Cells

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 Pigment Epithelium-Derived Factor Released by Müller Glial Cells Exerts Neuroprotective Effects on Retinal Ganglion Cells

2012 ◽  
Vol 37 (7) ◽  
pp. 1524-1533 ◽  
Author(s):  
Jan Darius Unterlauft ◽  
Wolfram Eichler ◽  
Konstantin Kuhne ◽  
Xiu Mei Yang ◽  
Yousef Yafai ◽  
...  
Keyword(s):  
Retinal Ganglion Cells ◽  
Glial Cells ◽  
Ganglion Cells ◽  
Pigment Epithelium ◽  
Retinal Ganglion ◽  
Neuroprotective Effects ◽  
Müller Glial Cells ◽  
Pigment Epithelium Derived Factor

Melatonin As a Modulator of Degenerative and Regenerative Signaling Pathways in Injured Retinal Ganglion Cells

2019 ◽  
Vol 25 (28) ◽  
pp. 3057-3073 ◽  
Author(s):  
Kobra B. Juybari ◽  
Azam Hosseinzadeh ◽  
Habib Ghaznavi ◽  
Mahboobeh Kamali ◽  
Ahad Sedaghat ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Mitochondrial Dysfunction ◽  
Signaling Pathways ◽  
Retinal Ganglion Cells ◽  
Molecular Mechanisms ◽  
Nitrosative Stress ◽  
Ganglion Cells ◽  
Axon Growth ◽  
Nerve Fibers ◽  
Retinal Ganglion

Optic neuropathies refer to the dysfunction or degeneration of optic nerve fibers caused by any reasons including ischemia, inflammation, trauma, tumor, mitochondrial dysfunction, toxins, nutritional deficiency, inheritance, etc. Post-mitotic CNS neurons, including retinal ganglion cells (RGCs) intrinsically have a limited capacity for axon growth after either trauma or disease, leading to irreversible vision loss. In recent years, an increasing number of laboratory evidence has evaluated optic nerve injuries, focusing on molecular signaling pathways involved in RGC death. Trophic factor deprivation (TFD), inflammation, oxidative stress, mitochondrial dysfunction, glutamate-induced excitotoxicity, ischemia, hypoxia, etc. have been recognized as important molecular mechanisms leading to RGC apoptosis. Understanding these obstacles provides a better view to find out new strategies against retinal cell damage. Melatonin, as a wide-spectrum antioxidant and powerful freeradical scavenger, has the ability to protect RGCs or other cells against a variety of deleterious conditions such as oxidative/nitrosative stress, hypoxia/ischemia, inflammatory processes, and apoptosis. In this review, we primarily highlight the molecular regenerative and degenerative mechanisms involved in RGC survival/death and then summarize the possible protective effects of melatonin in the process of RGC death in some ocular diseases including optic neuropathies. Based on the information provided in this review, melatonin may act as a promising agent to reduce RGC death in various retinal pathologic conditions.

Differences in nitric oxide production: a comparison of retinal ganglion cells and retinal glial cells cultured under hypoxic conditions

2003 ◽  
Vol 112 (1-2) ◽  
pp. 126-134 ◽  
Author(s):  
Kenji Kashiwagi ◽  
Yoko Iizuka ◽  
Seiichi Mochizuki ◽  
Yuichi Tsumamoto ◽  
Hiromu K Mishima ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Retinal Ganglion Cells ◽  
Glial Cells ◽  
Ganglion Cells ◽  
Nitric Oxide Production ◽  
Retinal Ganglion ◽  
Oxide Production ◽  
Hypoxic Conditions ◽  
Cells Cultured

Intravitreal macrophage activation enables cat retinal ganglion cells to regenerate injured axons into the mature optic nerve

2005 ◽  
Vol 196 (1) ◽  
pp. 153-163 ◽  
Author(s):  
T OKADA ◽  
M ICHIKAWA ◽  
Y TOKITA ◽  
H HORIE ◽  
K SAITO ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Retinal Ganglion Cells ◽  
Macrophage Activation ◽  
Ganglion Cells ◽  
Retinal Ganglion

scholarly journals Photoreceptive retinal ganglion cells control the information rate of the optic nerve

2018 ◽  
Vol 115 (50) ◽  
pp. E11817-E11826 ◽  
Author(s):  
Nina Milosavljevic ◽  
Riccardo Storchi ◽  
Cyril G. Eleftheriou ◽  
Andrea Colins ◽  
Rasmus S. Petersen ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Retinal Ganglion Cells ◽  
Information Flow ◽  
Information Transfer ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Ambient Light ◽  
Visual Responses ◽  
Light Irradiance ◽  
The Brain

Information transfer in the brain relies upon energetically expensive spiking activity of neurons. Rates of information flow should therefore be carefully optimized, but mechanisms to control this parameter are poorly understood. We address this deficit in the visual system, where ambient light (irradiance) is predictive of the amount of information reaching the eye and ask whether a neural measure of irradiance can therefore be used to proactively control information flow along the optic nerve. We first show that firing rates for the retina’s output neurons [retinal ganglion cells (RGCs)] scale with irradiance and are positively correlated with rates of information and the gain of visual responses. Irradiance modulates firing in the absence of any other visual signal confirming that this is a genuine response to changing ambient light. Irradiance-driven changes in firing are observed across the population of RGCs (including in both ON and OFF units) but are disrupted in mice lacking melanopsin [the photopigment of irradiance-coding intrinsically photosensitive RGCs (ipRGCs)] and can be induced under steady light exposure by chemogenetic activation of ipRGCs. Artificially elevating firing by chemogenetic excitation of ipRGCs is sufficient to increase information flow by increasing the gain of visual responses, indicating that enhanced firing is a cause of increased information transfer at higher irradiance. Our results establish a retinal circuitry driving changes in RGC firing as an active response to alterations in ambient light to adjust the amount of visual information transmitted to the brain.

Different optic nerve injury sites result in different responses of retinal ganglion cells to brain-derived neurotrophic factor but not neurotrophin-4/5

2005 ◽  
Vol 1047 (2) ◽  
pp. 224-232 ◽  
Author(s):  
Ye Zhi ◽  
Qiang Lu ◽  
Cheng-Wu Zhang ◽  
Henry K. Yip ◽  
Kwok-Fai So ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Nerve Injury ◽  
Retinal Ganglion Cells ◽  
Neurotrophic Factor ◽  
Ganglion Cells ◽  
Brain Derived Neurotrophic Factor ◽  
Retinal Ganglion ◽  
Optic Nerve Injury

scholarly journals Axons of retinal ganglion cells are insulted in the optic nerve early in DBA/2J glaucoma

2007 ◽  
Vol 179 (7) ◽  
pp. 1523-1537 ◽  
Author(s):  
Gareth R. Howell ◽  
Richard T. Libby ◽  
Tatjana C. Jakobs ◽  
Richard S. Smith ◽  
F. Campbell Phalan ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Mouse Model ◽  
Retinal Ganglion Cells ◽  
Strong Evidence ◽  
Ganglion Cells ◽  
Lamina Cribrosa ◽  
Retinal Ganglion ◽  
Rich Region ◽  
Pattern Electroretinography ◽  
Axon Damage

Here, we use a mouse model (DBA/2J) to readdress the location of insult(s) to retinal ganglion cells (RGCs) in glaucoma. We localize an early sign of axon damage to an astrocyte-rich region of the optic nerve just posterior to the retina, analogous to the lamina cribrosa. In this region, a network of astrocytes associates intimately with RGC axons. Using BAX-deficient DBA/2J mice, which retain all of their RGCs, we provide experimental evidence for an insult within or very close to the lamina in the optic nerve. We show that proximal axon segments attached to their cell bodies survive to the proximity of the lamina. In contrast, axon segments in the lamina and behind the eye degenerate. Finally, the Wlds allele, which is known to protect against insults to axons, strongly protects against DBA/2J glaucoma and preserves RGC activity as measured by pattern electroretinography. These experiments provide strong evidence for a local insult to axons in the optic nerve.

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