Abstract
Presentation Description :
Melatonin is synthesized by the retinal photoreceptors of many vertebrate species via a well-defined biosynthetic pathway. Melatonin produced by the retina is thought to act as a local neuromodulator within the eye. Melatonin exerts its influence by binding to G protein-coupled receptors named melatonin receptor type 1 (MT1) and type 2 (MT2). MT1 and MT2 receptors activate a wide variety of signaling pathways and both receptors are present in the vertebrate photoreceptors where they may form MT1/MT2 heteromers (MT1/2h). Previous studies in rodents (mice and rats) have demonstrated that melatonin may play an important role in protecting photoreceptors from apoptosis and melatonin signaling is involved in the modulation of photoreceptor viability during aging. A few studies in humans have implicated melatonin in the pathogenesis of age-related macular degeneration. Our recent work using melatonin-proficient mice (C3H-f+/+) and melatonin-proficient mice lacking melatonin receptors (MT1 or MT2) has shown that in melatonin receptors knock-out mice the number of cone photoreceptors is signigicantly reduced respect to what observed in control mice. Additional studies studies in mice and in 661W cells have indicated that the mechanisms by which melatonin signaling protects photoreceptors involves the modulation of AKT-FOXO1 cell survival pathway.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.