A comparison of some organizational characteristics of the mouse central retina and the human macula.
Mouse models have greatly assisted our understanding of retinal degenerations. However, the mouse retina does not have a macula, leading to the question of whether the mouse is a relevant model for macular degeneration. In the present study, a quantitative comparison between the organization of the central mouse retina and the human macula was made, focusing on some structural characteristics that have been suggested to be important in predisposing the macula to stresses leading to degeneration: photoreceptor density, phagocytic load on the RPE, and the relative thinness of Bruch's membrane. Light and electron microscopy measurements from retinas of two strains of mice, together with published data on human retinas, were used for calculations and subsequent comparisons. As in the human retina, the central region of the mouse retina possesses a higher photoreceptor cell density and a thinner Bruch's membrane than in the periphery; however, the magnitudes of these periphery to center gradients are larger in the human. Of potentially greater relevance is the actual photoreceptor cell density, which is much greater in the mouse central retina than in the human macula, underlying a higher phagocytic load for the mouse RPE. Moreover, at eccentricities that correspond to the peripheral half of the human macula, the rod to cone ratio is similar between mouse and human. Hence, with respect to photoreceptor density and phagocytic load of the RPE, the central mouse retina models at least the more peripheral part of the macula, where macular degeneration is often first evident.
Departments of Ophthalmology and Neurobiology, Stein Eye Institute, Molecular Biology Institute, Brain Research Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States of America.
Stefanie
S
Volland
Departments of Ophthalmology and Neurobiology, Stein Eye Institute, Molecular Biology Institute, Brain Research Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States of America.
Julian
J
Esteve-Rudd
Departments of Ophthalmology and Neurobiology, Stein Eye Institute, Molecular Biology Institute, Brain Research Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States of America.
Juyea
J
Hoo
Departments of Ophthalmology and Neurobiology, Stein Eye Institute, Molecular Biology Institute, Brain Research Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States of America.
Claudine
C
Yee
Departments of Ophthalmology and Neurobiology, Stein Eye Institute, Molecular Biology Institute, Brain Research Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States of America.
David S
DS
Williams
D000375:Aging / Q000473:pathology; D000818:Animals; D016570:Bruch Membrane / Q000503:physiopathology; D004195:Disease Models, Animal; D006801:Humans; D008266:Macula Lutea / Q000503:physiopathology* / Q000648:ultrastructure; D008268:Macular Degeneration / Q000503:physiopathology*; D051379:Mice; D008854:Microscopy, Electron; D010857:Pigment Epithelium of Eye / Q000503:physiopathology; D012160:Retina / Q000503:physiopathology* / Q000648:ultrastructure; D012162:Retinal Degeneration / Q000503:physiopathology*