The broad objective of this project is to elucidate mechanisms that mediate glial cell responses to pathophysiological conditions in the human retina. A long-term goal is to understand the function of ion channels in regulating the responses of retinal glial cells to changes in the extracellular environment. A working hypothesis is that the activation of certain ion channels may play a role in mediating responses of retinal glial cells to pathological conditions causing depolarization. Attention is focused on depolarization-sensitive pathways for an influx of calcium. Pathways for calcium influx are of importance because an elevation of intracellular calcium levels may be a vital link in the response of retinal glial cells to perturbations in their extracellular environment.
The specific aims are to study voltage-gated calcium channels and N-methyl-D-aspartate (NMDA) channels in human retinal glial cells. Experiments involve the use of the patch-clamp technique to analyze the physiology, pharmacology and regulation of these channels in cultured human retinal glial cells and in freshly dissociated Muller cells from postmortem donors. Knowledge of the mechanisms by which cells of the retina respond to abnormal conditions is likely to help in eventually devising therapies that enhance beneficial responses and diminish detrimental ones so as to prevent irreversible retinal damage.
| Burd, E M; Pulido, J S; Puro, D G et al. (1996) Maintenance of replicative intermediates in ganciclovir-treated human cytomegalovirus-infected retinal glia. Arch Ophthalmol 114:856-61 |
| Burd, E M; Pulido, J S; Puro, D G et al. (1996) Replication of human cytomegalovirus in human retinal glial cells. Invest Ophthalmol Vis Sci 37:1957-66 |
