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

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. An important piece of unfinished business is to characterize the array of retinal ganglion cells. We are seeking a complete characterization of the array of ganglion cells present in the mouse. It is clear that ganglion cells come in at least 20 different types, each carrying a different transformation of the visual scene to the brain. As they define the fundamental elements from which visual perception is built, identification of the set of retinal ganglion cells is critical to understanding how the higher visual centers work.

With this background, a more recent concern is with the pathophysiology of ganglion cell degeneration in glaucoma. This work is being done in collaboration with Dr. Tatjana Jakobs, Assistant Professor of Ophthalmology, who has primary responsibility for its management. 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.

Last Update: 5/12/2014


For a complete listing of publications click here.



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