Glaucoma is the leading cause of irreversible blindness and in 2040, more than 111 million people are expected to have the disease. Vision loss in glaucoma is caused by the death of retinal ganglion cells (RGCs) primarily in the optic nerve head (ONH). Elevated intraocular pressure (IOP) is a well-known causative risk factor for glaucoma, highlighting the importance of biomechanics in the disease. All current therapies are focused on lowering IOP levels. However, these therapies are not effective for all patients. One limiting factor in the search for new therapies is the lack of knowledge about the cell processes that lead from biomechanical insult to RGC apoptosis. To better understand this relationship, animal models are used and amongst these models, rats are widely-used due to their pathophysiological similarities to human glaucoma. However, there are anatomical differences between the rat and human ONH, and these differences are likely to affect rat ONH biomechanics. Moreover, there are some anatomical alterations occur in the rat ONH due to remodeling and damage in the early stages of the disease. Computational modeling is a suitable approach for characterizing ONH biomechanics due to the complex anatomy of the posterior rat eye and there has been no previous attempt to characterize the glaucomatous rat eye ONH biomechanics. The aim of this thesis is to characterize glaucomatous rat ONH biomechanics by building two individual-specific glaucomatous rat ONH finite element models (FEMs). By comparing the 1st (mean and the 95th percentile) and 3rd (mean and the 5th percentile) principal strains on the anterior ON with previously built healthy rat eye individual-specific FEMs, the effect of geometrical differences occurred due to remodeling and damage in the early stages of the glaucoma were aimed to be better understood. The 1st principal strain (mean and 95th percentile) relative percentage differences between the glaucomatous and healthy rat eyes under the IOP of 30mmHg were found to be 37.74% and 69.66% for the MR04, and 35.66% and 66.02% for the MR05 rats. The 3rd principal strain (mean and 5th percentile) relative percentage differences were found to be 12.28% and 35.23% for the MR04, and 10.31% and 11.05% for the MR05 rats, in which the glaucomatous rat eyes had higher magnitude strains. When the experimentally measured mean IOP values were applied to the glaucomatous rat eye models, these calculated relative percentage differences were increased. Moreover, when the strain patterns in the anterior ON were observed, larger strains were located in the inferior ON in both of the glaucomatous rat eyes. Thus, the localization of high strain patterns observed in this study for the glaucomatous eyes were similar to the healthy rat eyes, which were dominantly located at the inferior ON. However, the magnitudes of the principal strains in the glaucomatous rat eye anterior ON were elevated due to the geometrical differences caused by remodeling and damage during the early stages of the disease.