Understanding the mechanisms behind the loss and recovery of vision following retinal detachment and reattachment has been the focus of our studies for many years. In the normal retina, the light sensitive outer segments of the photoreceptor cells are interdigitated with the highly specialized apical processes of the retinal pigment epithelial cells. Numerous cellular and molecular interactions occur across this interface, including the transport of oxygen and nutrients. The physical separation of these 2 layers (retinal detachment) is a serious cause of visual impairment in humans and can result from many different causes including trauma, retinal tears, and complications from diseases of the eye. For many years, photoreceptor outer segment degeneration was considered the primary effect of detachment and their imperfect regeneration the most likely cause of continued visual defects after successful reattachment. What we have learned, however, is that detachment leads to a number of other cellular events including: photoreceptor cell death, Müller cell proliferation and hypertrophy, remodeling of photoreceptor synaptic terminals and a concomitant outgrowth of neurites from second- and third-order neurons. These events, which have their beginnings within minutes of creating the detachment and continue for as long as the retina remains detached, most likely contribute to the degree of visual recovery following reattachment surgery.

     Retinal reattachment may be thought of in a simplistic way of returning the retina to a "normal" configuration. Our most recent studies of reattachment in animal models and comparisons to human reattachments indicate that this is almost certainly not true. We have shown that early reattachment can stop or slow many of the detrimental changes initiated by detachment, however, once initiated, many of these changes, in particular the "plastic" changes observed in some neurons, do not immediately return to normal. In addition, reattachment appears to initiate an entirely new set of potentially deleterious cellular responses not observed in the detached retina. Because of this we have begun examining the use of various supplemental agents given during detachment to aid in the recovery of the retina. Two agents, brain derived neurotrophic factor and oxygen, have shown promise in achieving this goal. Other projects in the lab include examining detached retinas from humans, pursuing a model of retinal detachment in a cone dominant retina, assessing the functional recovery of the retina using electrophysiological techniques, and examining the response of the retina in mice that have had specific genes altered.

For review see "Cellular Remodeling in Mammalian Retina Induced by Retinal Detachment" in Webvision.