The expression of light-sensitive microbial opsins is a promising mutation-independent approach to restore vision in retinal degenerative diseases. Using viral vectors, optogenetic tools can be genetically expressed in various subpopulations of retinal neurons. The choice of cell type depends on the availability of surviving retinal cells. If cones are still alive but they lack outer segments, they can be targeted with optogenetic inhibitors, such as halorhodopsin. Alternatively, it is possible to bypass the photoreceptors and to target bipolar cells. In late-stage degeneration, when bipolar cells degenerate, \"artificial photoreceptors\" can be made from retinal ganglion cells, but with this approach, upstream retinal processing cannot be utilized. However, when ganglion cells are stimulated directly, higher brain regions might be able to compensate for some loss of retinal processing, which is indicated by clinical studies with epiretinal implants, where patients can perform simple visual tasks. Finally, optogenetics in combination with neuroprotective approaches could serve as a valuable strategy to restore the function of remaining cells, as well as to rescue retinal neurons from progressive degeneration.

The peptide somatostatin is one of many neuroactive agents that influence retinal physiology. It is synthesized primarily in a subclass of amacrine cells and believed to function as a neurotransmitter, neuromodulator or trophic factor. The cloning of the somatostatin receptors (sst1-5) in the early nineties provided the appropriate tools for the study of ssts in many tissues, including the retina. In this review, emphasis is given to recent studies that have provided significant information on the functional role of somatostatin in retinal circuitry and the retinal pigment epithelium. The important role of somatostatin in retinal disease therapeutics is also discussed.