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Neuroinflammatory Mechanisms of Axonal Degeneration in Optic Neuropathies

David J. Calkins
Dept. Ophthalmology and Visual Sciences
1115 Light Hall-MRBIV
2215B Garland Avenue
615-936-6412 (office)
615-936-6410 (fax)
david.j.calkins@vanderbilt.edu

Optic neuropathies blind through the progressive degeneration of the retina and optic nerve. As with other diseases of the central nervous system, optic neuropathies involve complex interactions between glial cells and retinal neurons and their axons. These interactions comprise a broad inflammatory response that includes both protective mechanisms and cascades that contribute to programmed degeneration. Our laboratory focuses on neuronal-glial interactions in glaucoma, an optic neuropathy that is blinding some 80 million people worldwide. In glaucoma, sensitivity to pressure in the eye causes the slow retraction of the axons in the optic nerve, which arise from the roughly 1.5 million retinal ganglion cells that collect the light signals used for vision. We utilize both in vivo and in vitro models to isolate the inflammatory signals from microglia and astrocyte glia in the retina and optic nerve that contribute to ganglion cell death. We also focus on the molecular mechanisms intrinsic to ganglion cells and their axons that mediate their sensitivity to ocular pressure and could represent novel therapeutic targets.

Students working in our laboratory will receive training in many modern techniques in neuroscience, including primary neuronal cell culture, digital microscopy, quantitative real-time PCR, immunocytochemistry and ELISA. Students are also expected to participate in journal club and laboratory meetings on a regular basis.

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