Our laboratory studies the cellular and synaptic mechanisms of glaucomatous neurodegeneration. We are particularly interested in understanding the earliest steps of inner retina circuit disassembly in response to injury. Our research program combines imaging and analysis of specific cell and synaptic labels in the retina, rodent models of experimental glaucoma, novel genetic tools in which specific cell types are labeled, and the tools of molecular/cell biology and physiology to address a series of questions that, unanswered, have prevented progress in the field: 1) What are the early steps of compartmentalized neurodegeneration of the ganglion cell in glaucoma? 2) Are there specific ganglion cell types that are more susceptible to intraocular pressure (IOP) elevation? 3) Are there specific inner retinal circuits that are more susceptible to IOP elevation? As a clinician-scientist, I am motivated to advance our field not only by answering these fundamental questions, but also by translating the knowledge gained into improvements in diagnostic and treatment modalities in glaucoma. For example, a detailed understanding of the earliest structural and functional changes that occur in glaucoma will allow us to design treatments that can rescue RGCs, perhaps the most susceptible RGCs, before irreversible cell death occurs. Our long-term goal is to understand the mechanisms underlying ganglion cell degeneration and circuit remodeling in glaucoma in order to improve diagnosis and treatment.