title: Melanopsin ganglion cells are the most resistant retinal ganglion cell type to axonal injury in the rat retina.
abstract: We report that the most common retinal ganglion cell type that remains after optic nerve transection is the M1 melanopsin ganglion cell. M1 ganglion cells are members of the intrinsically photosensitive retinal ganglion cell population that mediates non-image-forming vision, comprising ∼2.5% of all ganglion cells in the rat retina. In the present study, M1 ganglion cells comprised 1.7±1%, 28±14%, 55±13% and 82±8% of the surviving ganglion cells 7, 14, 21 and 60 days after optic nerve transection, respectively. Average M1 ganglion cell somal diameter and overall morphological appearance remained unchanged in non-injured and injured retinas, suggesting a lack of injury-induced degeneration. Average M1 dendritic field size increased at 7 and 60 days following optic nerve transection, while average dendritic field size remained similar in non-injured retinas and in retinas at 14 and 21 days after optic nerve transection. These findings demonstrate that M1 ganglion cells are more resistant to injury than other ganglion cell types following optic nerve injury, and provide an opportunity to develop pharmacological or genetic therapeutic approaches to mitigate ganglion cell death and save vision following optic nerve injury.
authors.affiliation: Department of Neurobiology, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, California, United States of America.
authors.forename: Luis
authors.initials: L
authors.lastname: Pérez de Sevilla Müller
authors.affiliation: Department of Neurobiology, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, California, United States of America; Jules Stein Eye Institute, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, California, United States of America.
authors.forename: Allison
authors.initials: A
authors.lastname: Sargoy
authors.affiliation: Department of Neurobiology, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, California, United States of America.
authors.forename: Allen R
authors.initials: AR
authors.lastname: Rodriguez
authors.affiliation: Department of Neurobiology, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, California, United States of America; Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, California, United States of America; Jules Stein Eye Institute, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, California, United States of America; CURE Digestive Diseases Research Center, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, California, United States of America; Veterans Administration Greater Los Angeles Health System, Los Angeles, California, United States of America.
authors.forename: Nicholas C
authors.initials: NC
authors.lastname: Brecha
mesh_terms: D000818:Animals; D001369:Axons / Q000378:metabolism* / Q000473:pathology; D002470:Cell Survival; D008297:Male; D020221:Optic Nerve Injuries / Q000378:metabolism*; D017207:Rats, Sprague-Dawley; D012165:Retinal Ganglion Cells / Q000378:metabolism* / Q000473:pathology; D017299:Rod Opsins / Q000378:metabolism; D000099210:Melanopsin
chemical_list: D017299:Rod Opsins; D000099210:Melanopsin