Elevated levels of glutamate are known to kill retinal ganglion cells, and glutamate is found in high concentrations in the eyes of people and animals with glaucoma. The series of events that elevated glutamate triggers in retinal ganglion cells is not well understood, but it appears to be dependent on an influx of calcium ions into the cell. Dr. Keirstead is monitoring calcium concentration inside retinal ganglion cells before, during, and after optic nerve injury to determine if calcium increases as a result of axonal injury. She hypothesizes that axonal injury changes the way retinal ganglion cells regulate intracellular calcium, either by causing increases in calcium or by altering the ability of retinal ganglion cells to regulate calcium concentration. Using an in vivo technique she developed that mimics the clinical situation more closely than other techniques, she is monitoring calcium in real time with video imaging microscopy to provide a dynamic picture of the processes going on inside retinal ganglion cells. Dr. Keirstead is also examining support cells in the retina called Miller glial cells. She will examine the calcium responses of these cells to determine if they have any long-term functional changes in response to optic nerve injury that could adversely affect their support of retinal ganglion cells in pathological conditions. These experiments may provide a basis for the design of therapeutic protocols to prevent vision loss due to glaucoma. This project is a continuation of a BrightFocus-funded study by the same name, begun in 1999.
First published on: June 10, 2008
Last modified on: June 11, 2008