Nogo receptor 1 is expressed by nearly all retinal ganglion cells.
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A variety of conditions ranging from glaucoma to blunt force trauma lead to optic nerve atrophy. Identifying signaling pathways for stimulating axon growth in the optic nerve may lead to treatments for these pathologies. Inhibiting signaling by the nogo-66 receptor 1 (NgR1) promotes the re-extension of axons following a crush injury to the optic nerve, and while NgR1 mRNA and protein expression are observed in the retinal ganglion cell (RGC) layer and inner nuclear layer, which retinal cell types express NgR1 remains unknown. Here we determine the expression pattern of NgR1 in the mouse retina by co-labeling neurons with characterized markers of specific retinal neurons together with antibodies specific for NgR1 or Green Fluorescent Protein expressed under control of the ngr1 promoter. We demonstrate that more than 99% of RGCs express NgR1. Thus, inhibiting NgR1 function may ubiquitously promote the regeneration of axons by RGCs. These results provide additional support for the therapeutic potential of NgR1 signaling in reversing optic nerve atrophy.
Retinal Ganglion Cells
Optic Nerve Injuries
Green Fluorescent Proteins
Nogo Receptor 1
Published Version (Please cite this version)10.1371/journal.pone.0196565
Publication InfoField, Greg; Solomon, Alexander M; Westbrook, Teleza; & McGee, Aaron W (2018). Nogo receptor 1 is expressed by nearly all retinal ganglion cells. PloS one, 13(5). pp. e0196565. 10.1371/journal.pone.0196565. Retrieved from https://hdl.handle.net/10161/17866.
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Assistant Professor of Neurobiology
My laboratory studies how the retina processes visual scenes and transmits this information to the brain. We use multi-electrode arrays to record the activity of hundreds of retina neurons simultaneously in conjunction with transgenic mouse lines and chemogenetics to manipulate neural circuit function. We are interested in three major areas. First, we work to understand how neurons in the retina are functionally connected. Second we are studying how light-adaptation and circadian rhythms a