Chronic mild and acute severe glaucomatous neurodegeneration derived from silicone oil-induced ocular hypertension

Recently, we established silicone oil-induced ocular hypertension (SOHU) mouse model with significant glaucomatous neurodegeneration. Here we characterize two additional variations of this model that simulate two distinct glaucoma types. The first is a chronic model produced by high frequency (HF) pupillary dilation after SO-induced pupillary block, which shows sustained moderate IOP elevation and corresponding slow, mild glaucomatous neurodegeneration. We also demonstrate that although SO removal quickly returns IOP to normal, the glaucomatous neurodegeneration continues to advance to a similar degree as in the HF group without SO removal. The second, an acute model created by no pupillary dilation (ND), shows a greatly elevated IOP and severe inner retina degeneration at an early time point. Therefore, by a straightforward dilation scheme, we extend our original SOHU model to recapitulate phenotypes of two major glaucoma forms, which will be invaluable for selecting neuroprotectants and elucidating their molecular mechanisms.

Automated summary

We established a silicone oil-induced ocular hypertension (SOHU) mouse model to simulate two distinct glaucoma types: a chronic model with sustained moderate IOP elevation and mild neurodegeneration, and an acute model with greatly elevated IOP and severe inner retina degeneration. Despite SO removal quickly normalizing IOP, glaucomatous neurodegeneration continued to advance in both models. This expanded model will assist in selecting neuroprotectants and understanding their molecular mechanisms.