RT Journal Article
SR Electronic
T1 Cell-Subtype-Specific Remodeling of Intrinsically Photosensitive Retinal Ganglion Cells in Streptozotocin-Induced Diabetic Mice
JF Diabetes
JO Diabetes
FD American Diabetes Association
SP db200775
DO 10.2337/db20-0775
A1 Chen, Wei-Yi
A1 Han, Xu
A1 Cui, Ling-Jie
A1 Yu, Chen-Xi
A1 Sheng, Wen-Long
A1 Yu, Jun
A1 Yuan, Fei
A1 Zhong, Yong-Mei
A1 Yang, Xiong-Li
A1 Weng, Shi-Jun
YR 2021
UL http://diabetes.diabetesjournals.org/content/early/2021/02/11/db20-0775.abstract
AB 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.