СПОСОБЫ МОДЕЛИРОВАНИЯ ГЛАУКОМНОЙ ОПТИЧЕСКОЙ НЕЙРОПАТИИ В ЭКСПЕРИМЕНТЕ НА КРЫСАХ

Experimental in vivo glaucoma models allow expanding the knowledge of the glaucomatous optic neuropathy pathogenesis. An important criterion of choosing an experimental animal model is the ability to extrapolate received data to humans. This review covers main models of experimental glaucoma in rodents and its technology, including rodent anatomy and physiology specifics. Using rats in glaucoma modeling offers the advantage of fast disease progression and ease of use. Genetic models are based on congenital impairment of intraocular hydrodynamics due to gene mutation; induced models refer to artificial intraocular pressure (IOP) elevation or initiation of neuropathy without affecting the aqueous outflow. Methods aimed at hydrodynamics alteration lead to IOP increase and thus to glaucomatous optic neuropathy development. These include thermic, mechanical and laser effects on the aqueous humor outflow. Optic neuropathy without affecting IOP can be caused by mechanical impairment of the optic nerve, ischemia followed by reperfusion, excitotoxicity, or intravitreal injection of endothelin-1 or rose bengal with following photostimulation. Genetic glaucoma models include rodents with congenital impairment of eye drainage zone due to gene mutations, such as DBA gene family and α1-subunits of I-type collagen mutation, synthesis of altered myocilin or calcitonin receptorlike receptor expression. The current range of rodent glaucoma modelling methods is a perspective and important part of in vivo studies, related to glaucoma pathogenesis and treatment.