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

Recent evidence suggests that melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs), a neuronal class regulating nonimage forming (NIF) vision and generally thought to be injury resistant, are dysfunctional in certain neurodegenerative diseases. Although disrupted NIF vi...

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Published inDiabetes (New York, N.Y.) Vol. 70; no. 5; pp. 1157 - 1169
Main Authors Chen, Wei-Yi, Han, Xu, Cui, Ling-Jie, Yu, Chen-Xi, Sheng, Wen-Long, Yu, Jun, Yuan, Fei, Zhong, Yong-Mei, Yang, Xiong-Li, Weng, Shi-Jun
Format Journal Article
LanguageEnglish
Published United States American Diabetes Association 01.05.2021
Subjects
Capillaries
Cellular biology
Dendritic branching
Diabetes
Diabetes mellitus
Eyes & eyesight
Melanopsin
Neurodegenerative diseases
Retina
Retinal ganglion cells
Rodents
Streptozocin
Visual perception
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Summary:Recent evidence suggests that melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs), a neuronal class regulating nonimage 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.
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ISSN:0012-1797
1939-327X
DOI:10.2337/DB20-0775