scholarly journals Cell-Subtype-Specific Remodeling of Intrinsically Photosensitive Retinal Ganglion Cells in Streptozotocin-Induced Diabetic Mice

2021 ◽  
Author(s):  
Wei-Yi Chen ◽  
Xu Han ◽  
Ling-Jie Cui ◽  
Chen-Xi Yu ◽  
Wen-Long Sheng ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Retinal Ganglion Cells ◽  
Visual Function ◽  
Functional Activity ◽  
Ganglion Cells ◽  
Early Stage ◽  
Retinal Ganglion ◽  
Diabetic Mice ◽  
Pupillary Light ◽  
Dendritic Branching

Recent evidence suggests that melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs), a neuronal class regulating non-image forming (NIF) vision and generally thought to be injury-resistant, are dysfunctional in certain neurodegenerative diseases. Although disrupted NIF visual functions have been reported in patients and animals with diabetes, it remains controversial whether ipRGCs exhibit remodeling during diabetes and if so, whether such remodeling is variable among ipRGC subtypes. Here we demonstrate that survival, soma-dendritic profiles and melanopsin-based functional activity of M1 ipRGCs were unaltered in streptozotocin-induced 3-month diabetic mice. Such resistance remained at 6 months after streptozotocin administration. In contrast, M2/M3 ipRGCs underwent significant remodeling in diabetic mice, manifested by enlarged somata and increased dendritic branching complexity. Consistent with the unaltered melanopsin levels, the sensitivity of melanopsin-based activity was unchanged in surviving M2 cells, but their response gain displayed a compensatory enhancement. Meanwhile, the pupillary light reflex, a NIF visual function controlled by M2 cells, was found to be impaired in diabetic animals. The resistance of M1 cells might be attributed to the adjacency of their dendrites to capillaries, which makes them less disturbed by the impaired retinal blood supply at the early stage of diabetes.

scholarly journals Cell-Subtype-Specific Remodeling of Intrinsically Photosensitive Retinal Ganglion Cells in Streptozotocin-Induced Diabetic Mice

2021 ◽  
Author(s):  
Wei-Yi Chen ◽  
Xu Han ◽  
Ling-Jie Cui ◽  
Chen-Xi Yu ◽  
Wen-Long Sheng ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Retinal Ganglion Cells ◽  
Visual Function ◽  
Functional Activity ◽  
Ganglion Cells ◽  
Early Stage ◽  
Retinal Ganglion ◽  
Diabetic Mice ◽  
Pupillary Light ◽  
Dendritic Branching

Recent evidence suggests that melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs), a neuronal class regulating non-image forming (NIF) vision and generally thought to be injury-resistant, are dysfunctional in certain neurodegenerative diseases. Although disrupted NIF visual functions have been reported in patients and animals with diabetes, it remains controversial whether ipRGCs exhibit remodeling during diabetes and if so, whether such remodeling is variable among ipRGC subtypes. Here we demonstrate that survival, soma-dendritic profiles and melanopsin-based functional activity of M1 ipRGCs were unaltered in streptozotocin-induced 3-month diabetic mice. Such resistance remained at 6 months after streptozotocin administration. In contrast, M2/M3 ipRGCs underwent significant remodeling in diabetic mice, manifested by enlarged somata and increased dendritic branching complexity. Consistent with the unaltered melanopsin levels, the sensitivity of melanopsin-based activity was unchanged in surviving M2 cells, but their response gain displayed a compensatory enhancement. Meanwhile, the pupillary light reflex, a NIF visual function controlled by M2 cells, was found to be impaired in diabetic animals. The resistance of M1 cells might be attributed to the adjacency of their dendrites to capillaries, which makes them less disturbed by the impaired retinal blood supply at the early stage of diabetes.

scholarly journals Cell-Subtype-Specific Remodeling of Intrinsically Photosensitive Retinal Ganglion Cells in Streptozotocin-Induced Diabetic Mice

2021 ◽  
Author(s):  
Ada Admin ◽  
Wei-Yi Chen ◽  
Xu Han ◽  
Ling-Jie Cui ◽  
Chen-Xi Yu ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Retinal Ganglion Cells ◽  
Visual Function ◽  
Functional Activity ◽  
Ganglion Cells ◽  
Early Stage ◽  
Retinal Ganglion ◽  
Diabetic Mice ◽  
Pupillary Light ◽  
Dendritic Branching

Recent evidence suggests that melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs), a neuronal class regulating non-image forming (NIF) vision and generally thought to be injury-resistant, are dysfunctional in certain neurodegenerative diseases. Although disrupted NIF visual functions have been reported in patients and animals with diabetes, it remains controversial whether ipRGCs exhibit remodeling during diabetes and if so, whether such remodeling is variable among ipRGC subtypes. Here we demonstrate that survival, soma-dendritic profiles and melanopsin-based functional activity of M1 ipRGCs were unaltered in streptozotocin-induced 3-month diabetic mice. Such resistance remained at 6 months after streptozotocin administration. In contrast, M2/M3 ipRGCs underwent significant remodeling in diabetic mice, manifested by enlarged somata and increased dendritic branching complexity. Consistent with the unaltered melanopsin levels, the sensitivity of melanopsin-based activity was unchanged in surviving M2 cells, but their response gain displayed a compensatory enhancement. Meanwhile, the pupillary light reflex, a NIF visual function controlled by M2 cells, was found to be impaired in diabetic animals. The resistance of M1 cells might be attributed to the adjacency of their dendrites to capillaries, which makes them less disturbed by the impaired retinal blood supply at the early stage of diabetes.

Cell-Subtype-Specific Remodeling of Intrinsically Photosensitive Retinal Ganglion Cells in Streptozotocin-Induced Diabetic Mice

Diabetes ◽  
2021 ◽  
pp. db200775
Author(s):  
Wei-Yi Chen ◽  
Xu Han ◽  
Ling-Jie Cui ◽  
Chen-Xi Yu ◽  
Wen-Long Sheng ◽  
...  
Keyword(s):  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Diabetic Mice ◽  
Cell Subtype

Retinal Ganglion Cells Functional Changes in a Mouse Model of Alzheimer’s Disease Are Linked with Neurotransmitter Alterations

2021 ◽  
pp. 1-14
Author(s):  
Joaquín Araya ◽  
Felipe Bello ◽  
Gaganashree Shivashankar ◽  
David Neira ◽  
Claudia Durán-Aniotz ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Firing Rate ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Early Stage ◽  
Retinal Ganglion ◽  
Gamma Aminobutyric Acid ◽  
Functional Changes ◽  
Model Of Alzheimer’S Disease

Background: Alzheimer’s disease (AD) is the most prevalent form of dementia worldwide. This neurodegenerative syndrome affects cognition, memory, behavior, and the visual system, particularly the retina. Objective: This work aims to determine whether the 5xFAD mouse, a transgenic model of AD, displays changes in the function of retinal ganglion cells (RGCs) and if those alterations are correlated with changes in the expression of glutamate and gamma-aminobutyric acid (GABA) neurotransmitters. Methods: In young (2–3-month-old) and adult (6-7-month-old) 5xFAD and WT mice, we have studied the physiological response, firing rate, and burst of RGCs to various types of visual stimuli using a multielectrode array system. Results: The firing rate and burst response in 5xFAD RGCs showed hyperactivity at the early stage of AD in young mice, whereas hypoactivity was seen at the later stage of AD in adults. The physiological alterations observed in 5xFAD correlate well with an increase in the expression of glutamate in the ganglion cell layer in young and adults. GABA staining increased in the inner nuclear and plexiform layer, which was more pronounced in the adult than the young 5xFAD retina, altering the excitation/inhibition balance, which could explain the observed early hyperactivity and later hypoactivity in RGC physiology. Conclusion: These findings indicate functional changes may be caused by neurochemical alterations of the retina starting at an early stage of the AD disease.

The Role of Heat Shock Proteins in the Mechanisms of Neurodegeneration and Neuroprotection in Primary Glaucoma: Literature Review

2021 ◽  
pp. 122-131
Author(s):  
N. S. Lutsenko ◽  
T. V. Nedilka
Keyword(s):  
Heat Shock ◽  
Heat Shock Proteins ◽  
Neurodegenerative Diseases ◽  
Retinal Ganglion Cells ◽  
Defense Mechanism ◽  
Ganglion Cells ◽  
The Body ◽  
Retinal Ganglion ◽  
Shock Proteins

Heat shock proteins (HSP) are important components of the defense mechanism that increases the survival of body cells in adverse conditions due to antiapoptotic and cytoprotective effects. Since their discovery, numerous studies and experimental models have proved the role of HSPs as a key link in the processes of both repair and coagulation of proteins, as well as in the protection of cells from oxidative stress. The potential for pharmacological induction of HSPs in the human body makes them an attractive therapeutic target for many neurodegenerative diseases. This review examines the role of HSPs, especially fraction 70, in the mechanisms of neuroprotection of retinal ganglion cells in primary open-angle glaucoma being one of the common neurodegenerative diseases that can lead to complete loss of visual functions. A number of studies have shown the protective effect of HSP70 on retinal ganglion cells in animals with artificially induced glaucoma. But in the course of experiments on animal models, it was also proved that direct immunization with HSP through intravitreal injections induced pressure-independent degeneration of retinal ganglion cells. This indicates the need for indirect stimulation of HSP70 in order to activate their neuroprotective properties. To date, there are insufficient data on the circulation of HSP70 in the body of a person with glaucoma. These data indicate the prospects for further study of the role of HSP70 in glaucoma degeneration and elucidation of the ways of their mediated induction. Keywords: heat shock protein, HSP70, glaucoma, ganglion cells, retina, neuroprotection.

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