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TRPC5 regulates axonal outgrowth in developing retinal ganglion cells
Mai Oda1, Hanako Yamamoto1, Hidetaka Matsumoto2
1Department of Molecular and Cellular Neurobiology, Gunma University Graduate School of Medicine, Maebashi, 371-8511, Japan.
Laboratory Investigation; a Journal of Technical Methods and Pathology
|December 18, 2019
Summary
The TRPC5 ion channel negatively regulates retinal ganglion cell (RGC) axonal outgrowth. TRPC5 may also play a role in RGCs
Area of Science:
- Neuroscience
- Cell Biology
- Ophthalmology
Background:
- TRPC5 ion channels are activated by various stimuli and are present in the central nervous system.
- Previous studies indicated TRPC5 expression in chick retinal amacrine and Müller glial cells.
- The role of TRPC5 in retinal ganglion cells (RGCs) remained unclear.
Purpose of the Study:
- To investigate TRPC5 expression in developing and mature mouse RGCs.
- To determine the function of TRPC5 in RGC axonal outgrowth.
- To explore TRPC5's potential role in glaucoma pathogenesis.
Main Methods:
- In situ hybridization and immunostaining in developing mouse retinas.
- Inhibition and overexpression of TRPC5 in developing RGCs.
- Analysis of RGC axon length and neurite remodeling.
Main Results:
- TRPC5 is strongly expressed in developing and mature RGCs, beginning at E14.5.
- Inhibition of TRPC5 increased RGC axon length, while overexpression inhibited it.
- TRPC5 acts as a negative regulator of RGC axonal outgrowth and neurite remodeling.
Conclusions:
- TRPC5 is a key negative regulator of RGC axonal outgrowth.
- TRPC5's mechanosensory role suggests involvement in intraocular pressure sensing and RGC death in glaucoma.
- TRPC5 influences neurite remodeling, potentially contributing to RGC pathology.
