With a global prevalence of 3.54% for a population aged 40-80 years and projections indicating worldwide affliction numbers increasing to 76 million people by 2020, glaucoma undoubtedly remains the leading cause of irreversible blindness worldwide (Tham et al., 2014). The research I have conducted over the past five years in the field of glaucoma has demonstrated that anterograde axonal transport loss occurs before retrograde transport deficits are seen and semifunctional RGC axons persist in the DBA/2J mouse model of glaucoma for much longer than previously thought (Dengler-Crish et al., 2014). While axons and synapses of the retinal projection are present after transport loss (Dengler-Crish et al., 2014; Crish et al., 2013), it is unclear from an ultrastructural perspective how morphologically intact and/or different these connections are. Furthermore, axonal elements such as nodes of Ranvier (NOR), and synaptic elements such as active zones, maintain strict morphometric and molecular composite standards. Apparent minor modifications to any of these elements can have major ramifications on normal function of the neural unit. However, very little is known about the relationship between axonal abnormalities and synaptic structure defects, in glaucoma. To clarify these relationships, my thesis work has examined the ultrastructure of RGC terminals in the neuropil of the superior colliculus, the morphometry and composition of NORs, as well as, axon size and cytoskeletal matrices in the optic nerve of a naturally occurring glaucomatous mouse model.