| First Author | Honda S | Year | 2019 |
| Journal | Invest Ophthalmol Vis Sci | Volume | 60 |
| Issue | 12 | Pages | 3696-3707 |
| PubMed ID | 31487370 | Mgi Jnum | J:278990 |
| Mgi Id | MGI:6360001 | Doi | 10.1167/iovs.19-27145 |
| Citation | Honda S, et al. (2019) Survival of Alpha and Intrinsically Photosensitive Retinal Ganglion Cells in NMDA-Induced Neurotoxicity and a Mouse Model of Normal Tension Glaucoma. Invest Ophthalmol Vis Sci 60(12):3696-3707 |
| abstractText | Purpose: We assess if alpha retinal ganglion cells (alphaRGCs) and intrinsically photosensitive retinal ganglion cells (ipRGCs) survive in mouse models of glaucoma. Methods: Two microliters of N-methyl-D-aspartate (NMDA; 1 mM) or PBS were injected intraocularly 7 days before sacrifice. Immunohistochemical analyses of the retina were performed using antibodies against RNA-binding protein with multiple splicing (RBPMS), osteopontin, and melanopsin. Immunohistochemical analyses also were performed in adult mice with glutamate/aspartate transporter (GLAST) deletion (GLAST knockout [KO] mice), a mouse model of normal tension glaucoma. Results: NMDA-induced loss of RBPMS-positive total RGCs was 58.4% +/- 0.4% compared to PBS-treated controls, whereas the loss of osteopontin-positive alphaRGCs was 5.0% +/- 0.6% and that of melanopsin-positive ipRGCs was 7.6% +/- 1.6%. In GLAST KO mice, the loss of total RGCs was 48.4% +/- 0.9% compared to wild-type mice, whereas the loss of alphaRGCs and ipRGCs was 3.9% +/- 0.4% and 9.3% +/- 0.5%, respectively. The distribution of survived total RGCs, alphaRGCs, and ipRGCs was similar regardless of the location of the retina. Conclusions: These results suggest that alphaRGC and ipRGC are highly tolerant to NMDA-induced neurotoxicity and NTG-like neurodegeneration in GLAST KO mice. |
