Vadim Y. Arshavsky, PhD, Principal Investigator
- Associate Professor, Ophthalmology, Harvard University 1995 - 2005
- Associate Researcher, Molecular Biology, University of Wisconsin at Madison 1989 - 1995
- Research Scientist, Biology, Lomonosov Moscow State University (Russia) 1981 - 1990
- Ph.D., Lomonosov Moscow State Universty (Russia) 1987
- B.S., Lomonosov Moscow State Universty (Russia) 1981
The biology of vertebrate photoreceptor cells
We are interested in molecular mechanisms underlying signal transduction, subcellular compartmentalization, and healthy state in vertebrate photoreceptor cells. Rod and cone photoreceptors are sensory neurons responsible for the detection and primary processing of information entering the eye in the form of photons of light. Photoreceptors capture photons, generate a second messenger signal, translate this signal into a change in electrical activity, and transmit this information to the secondary neurons in the retina through modulation of their synaptic release. Because the functional role of these cells is well defined and they are uniquely suitable to be studied using modern multi-disciplinary approaches, from biochemistry to genetics, photoreceptors represent an almost unmatched model system for addressing fundamental issues in molecular and cellular neuroscience, as well as cell signaling in general.
Currently, we pursue four major experimental directions. One is to understand molecular and cellular mechanisms responsible for targeting and trafficking of photoreceptor proteins. We are particularly interested in proteins comprising the light-sensitive organelle of the photoreceptor cell, the outer segment. Another direction is to conduct proteomic studies aiming to both identifying specific components of photoreceptor organelles and revealing novel patterns of protein-protein interactions. Our third direction relates to ocular pathobiology. We explore the novel concept that a major cellular stress factor contributing to photoreceptor cell death in multiple forms of retinal degenerative disorders is proteasomal overload, i.e. insufficient capacity of the ubiquitin-proteasome system to process abnormally large quantities of misfolded and/or mistrafficked proteins associated with these conditions. Our last direction expands beyond photoreceptors. We study the interplay between dopamine and GABA in dark adaptation of the highly light-sensitive rod channel of vision.