PiN Faculty Member - Richard Masland, PhD

Richard Masland, PhD

David G. Cogan Professor of Ophthalmology

Massachusetts Eye and Ear Infirmary
Room 501C
243 Charles St.
Boston, MA 2114
Tel: 617-391-5930
Fax: 617-391-5938
Email: richard_masland@meei.harvard.edu



Work in this laboratory concerns the normal cell biology of the neural retina, and its disorders.

We have  long been interested in the cell populations and synaptic interrelations of the retina. A number of cell types within the retina were discovered here, and we have been carrying out an attempt at the retina “neurome” – a listing of all of the cells present in the retina. To a first approximation, this project is complete. It reveals the retina as a multiply parallel system containing in excess of 60 cell types, which are organized into more than a dozen parallel informational channels. The retinal ganglion cells come in 15 to 30 different types, depending on how the counting is done. Each carries a different transformation of the visual scene to the brain.

With this background, a more recent concern is with the pathophysiology of ganglion cell degeneration in glaucoma. This work was originated in collaboration with Dr. Tatjana Jakobs, now Assistant Professor of Ophthalmology, who has taken over leadership of the lab and is now the principal investigator. The questions again focus on the retinal ganglion cells, this time in the context of their degeneration in disease. A particular interest is the relationship between the ganglion cell axons and the astrocytes that ensheath them at their point of exit from the eye. The lab has made or obtained transgenic mouse strains that allow direct visualization and molecular analysis of individual astrocytes during the remodeling that occurs after injury. Central questions are the signals that communicate between the optic axons and the glia, and the functional role – helpful or hurtful – of the glial reactivity that occurs after injury.

We are also interested in the optogenetic treatment of retinal photoreceptor degenerations. We have shown that rendering the surviving retinal neurons sensitive to light by ectopic expression of a light sensitive protein can restore some level of vision to animals blind from an inherited retinal degeneration. A human clinical trial of this strategy began in January 2016.



Last Update: 1/31/2017



Publications

For a complete listing of publications click here.

 


 



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