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Updated: Jul 2, 2026

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation
Published on: March 12, 2016
Loss of melanopsin-containing retinal ganglion cells in a rat glaucoma model
Huai-zhou Wang1, Qing-jun Lu, Ning-li Wang
1Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Background:
Glaucoma can cause progressive damage to retinal ganglion cells. These cells can be classified as cells projecting to the superior colliculus and melanopsin-containing retinal ganglion cells, which project to the suprachiasmatic nucleus. This study was to investigate the effects of chronic intraocular pressure elevation on melanopsin-containing retinal ganglion cells in rats.
Methods:
Chronic intraocular pressure elevation was induced in one eye of adult Wistar rats by cauterization of three episcleral veins. Intraocular pressure was measured at different intervals with a rebound tonometer. Superior collicular retinal ganglion cells were retrogradely labeled from the superior colliculus with Fluorogold. Melanopsin-containing retinal ganglion cells were visualized by free-floating immunohistochemistry on whole-mount retinas. The number of labeled superior collicular and melanopsin-containing retinal ganglion cells were counted in the sample areas on flat-mounted retinas.
Results:
Compared with contralateral control eyes, the numbers of both superior collicular and melanopsin-containing retinal ganglion cells were significantly reduced after 12 weeks of experimental intraocular pressure elevation ((2317.41 +/- 29.96)/mm(2) vs (1815.82 +/- 24.25)/mm(2); (26.20 +/- 2.10)/mm(2) vs (20.62 +/- 1.52)/mm(2), respectively). The extent of cell loss of the two types of retinal ganglion cells was similar. However, no morphologic changes were found in melanopsin-containing retinal ganglion cells.
Conclusion:
Both melanopsin-containing and superior collicular retinal ganglion cells were damaged by chronic ocular hypertension, indicating that glaucomatous neural degeneration involves the non-image-forming visual pathway.

