scholarly journals Transneuronal Degeneration in the Brain During Glaucoma

2021 ◽  
Vol 13 ◽  
Author(s):  
Mengling You ◽  
Rong Rong ◽  
Zhou Zeng ◽  
Xiaobo Xia ◽  
Dan Ji
Keyword(s):  
Visual Cortex ◽  
Ganglion Cells ◽  
Neuronal Damage ◽  
Current Knowledge ◽  
Retinal Ganglion ◽  
Optic Chiasma ◽  
Transneuronal Degeneration ◽  
Key Factor ◽  
Visual Cortex Neuron ◽  
Neuron Damage

The death of retinal ganglion cells (RGCs) is a key factor in the pathophysiology of all types of glaucoma, but the mechanism of pathogenesis of glaucoma remains unclear. RGCs are a group of central nervous system (CNS) neurons whose soma are in the inner retina. The axons of RGCs form the optic nerve and converge at the optic chiasma; from there, they project to the visual cortex via the lateral geniculate nucleus (LGN). In recent years, there has been increasing interest in the dysfunction and death of CNS and retinal neurons caused by transneuronal degeneration of RGCs, and the view that glaucoma is a widespread neurodegenerative disease involving CNS damage appears more and more frequently in the literature. In this review, we summarize the current knowledge of LGN and visual cortex neuron damage in glaucoma and possible mechanisms behind the damage. This review presents an updated and expanded view of neuronal damage in glaucoma, and reveals new and potential targets for neuroprotection and treatment.

Analysis of vertebrate eye movements following intravitreal drug injections. I. Blockade of retinal ON-cells by 2-amino-4-phosphonobutyrate eliminates optokinetic nystagmus

1988 ◽  
Vol 60 (3) ◽  
pp. 1010-1021 ◽  
Author(s):  
A. G. Knapp ◽  
M. Ariel ◽  
F. R. Robinson
Keyword(s):  
Visual Cortex ◽  
Eye Movements ◽  
Retinal Ganglion Cells ◽  
Optokinetic Nystagmus ◽  
Ganglion Cells ◽  
Directional Asymmetry ◽  
Retinal Ganglion ◽  
Binocular Stimulation ◽  
Vertebrate Eye ◽  
Stimulation Of

1. Horizontal optokinetic nystagmus (OKN) was examined in alert rabbits and cats following intravitreal injection of 2-amino-4-phosphonobutyrate (APB), an agent which selectively blocks the light-responsiveness of retinal ON-cells while having little effect on OFF-cells. The retinal actions of APB were assessed independently by electroretinography. 2. In five rabbits, doses of APB sufficient to eliminate the b-wave of the electroretinogram reduced drastically the ability of the injected eye to drive OKN at all stimulus speeds tested (1-96 degrees/s). Impairment of OKN was apparent within minutes of the injection, remained maximal for several hours, and recovered completely in 1-7 days. OKN in response to stimulation of the uninjected eye alone remained qualitatively and quantitatively normal. 3. Following administration of APB, OKN in response to binocular stimulation displayed a directional asymmetry. Stimuli moving in the preferred (temporal-to-nasal) direction for the uninjected eye became more effective than stimuli moving in the opposite direction, indicating that the injected eye could no longer contribute to binocular OKN. 4. When rabbits viewed stationary stimuli through the APB-treated eye alone, episodes of slow (less than 1 degrees/s) ocular drift were observed, similar to the positional instability seen when rabbits are placed in darkness or when the retinal image is stablized artifically (12). 5. APB had little effect on OKN in normal cats. In two cats that had previously received large lesions of the visual cortex, however, APB eliminated the ability of the injected eye to drive monocular OKN. The extent of the impairment was similar to that seen in rabbits. Because the cortex is thought to contribute more to OKN in cats than in rabbits, this result suggests that the optokinetic pathways disrupted by APB project subcortically. 6. This study demonstrates that the integrity of retinal ON-cells is required to sustain normal OKN. The results are consistent with additional anatomic and physiological evidence suggesting that a particular subclass of retinal ganglion cells, the ON-direction-selective cells, may provide a crucial source of visual input to central optokinetic pathways.

Transneuronal degeneration of retinal ganglion cells in early hemispherectomized monkeys

Neuroreport ◽  
1999 ◽  
Vol 10 (7) ◽  
pp. 1447-1452 ◽  
Author(s):  
Marc Herbin ◽  
Denis Boire ◽  
Hugo Théoret ◽  
Maurice Ptito
Keyword(s):  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Transneuronal Degeneration

scholarly journals Matrine protects retinal ganglion cells from apoptosis in experimental optic neuritis

2019 ◽  
Author(s):  
Jian Kang ◽  
Shu-Qing Liu ◽  
Yi-Fan Song ◽  
Meng-Ru Wang ◽  
Yao-Juan Chu ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Optic Nerve ◽  
Optic Neuritis ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Neuronal Damage ◽  
Disease Onset ◽  
High Dose ◽  
Retinal Ganglion ◽  
Autoimmune Encephalomyelitis

Abstract Background: Inflammatory demyelination and axonal injury of the optic nerve are hallmarks of optic neuritis (ON), which often occurs in multiple sclerosis and is a major cause of blindness in young adults. Although a high dose of corticosteroids can promote visual recovery, it cannot prevent permanent neuronal damage. Novel and effective therapies are thus required. Given the recently defined capacity of matrine (MAT), a quinolizidine alkaloid derived from the herb Radix Sophorae flavescens, in immunomodulation and neuroprotection, we tested in this study the effect of matrine on ON in rats with experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. Results: MAT administration, started at disease onset, significantly suppressed optic nerve infiltration and demyelination, with reduced numbers of Iba1+ macrophages/microglia and CD4+ T cells, compared to those from vehicle-treated rats. Increased expression of neurofilaments, an axon marker, and decreased apoptosis in retinal ganglion cells (RGCs) were also observed after MAT treatment. Conclusions: Taken as a whole, our results demonstrate that MAT attenuated inflammation, demyelination and axonal loss in the optic nerve, and protected RGCs from inflammation-induced cell death. MAT may therefore have potential as a novel treatment for this disease that causes blindness.

scholarly journals Matrine protects retinal ganglion cells from apoptosis in experimental optic neuritis

2020 ◽  
Author(s):  
Jian Kang ◽  
Shu-Qing Liu ◽  
Yi-Fan Song ◽  
Meng-Ru Wang ◽  
Yao-Juan Chu ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Optic Nerve ◽  
Optic Neuritis ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Neuronal Damage ◽  
Disease Onset ◽  
High Dose ◽  
Retinal Ganglion ◽  
Autoimmune Encephalomyelitis

Abstract Background: Inflammatory demyelination and axonal injury of the optic nerve are hallmarks of optic neuritis (ON), which often occurs in multiple sclerosis and is a major cause of blindness in young adults. Although a high dose of corticosteroids can promote visual recovery, it cannot prevent permanent neuronal damage. Novel and effective therapies are thus required. Given the recently defined capacity of matrine (MAT), a quinolizidine alkaloid derived from the herb Radix Sophorae flavescens, in immunomodulation and neuroprotection, we tested in this study the effect of matrine on ON in rats with experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. Results: MAT administration, started at disease onset, significantly suppressed optic nerve infiltration and demyelination, with reduced numbers of Iba1+ macrophages/microglia and CD4+ T cells, compared to those from vehicle-treated rats. Increased expression of neurofilaments, an axon marker, and decreased apoptosis in retinal ganglion cells (RGCs) were also observed after MAT treatment. Conclusions: Taken as a whole, our results demonstrate that MAT attenuated inflammation, demyelination and axonal loss in the optic nerve, and protected RGCs from inflammation-induced cell death. MAT may therefore have potential as a novel treatment for this disease that causes blindness.

scholarly journals A dedicated circuit links direction-selective retinal ganglion cells to the primary visual cortex

Nature ◽  
2014 ◽  
Vol 507 (7492) ◽  
pp. 358-361 ◽  
Author(s):  
Alberto Cruz-Martín ◽  
Rana N. El-Danaf ◽  
Fumitaka Osakada ◽  
Balaji Sriram ◽  
Onkar S. Dhande ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Retinal Ganglion Cells ◽  
Primary Visual Cortex ◽  
Ganglion Cells ◽  
Retinal Ganglion
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