Microglia in the primate macula: specializations in microglial distribution and morphology with retinal position and with aging

Microglia in the primate macula: specializations in microglial distribution and morphology with... Microglia, the principal resident immune cell in the retina, play constitutive roles in immune surveillance and synapse maintenance, and are also associated with retinal disease, including those occurring in the macula. Perspectives on retinal microglia function have derived largely from rodent models and how these relate to the macula-bearing primate retina is unclear. In this study, we examined microglial distribution and cellular morphology in the adult rhesus macaque retina, and performed comparative characterizations in three retinal locations along the center-to-periphery axis (parafoveal, macular, and the peripheral retina). We found that microglia density peaked in the parafoveal retina and decreased in the peripheral retina. Individual microglial morphology reflected macular specialization, with macular microglia demonstrating the largest and most complex dendritic arbors relative to other retinal locations. Comparing retinal microglia between young and middle-aged animals, microglial density increased in the macular, but not in the peripheral retina with age, while microglial morphology across all locations remained relatively unchanged. Our findings indicate that microglial distribution and morphology demonstrate regional specialization in the retina, correlating with gradients of other retinal cell types. As microglia are innate immune cells implicated in age-related macular diseases, age-related microglial changes may be related to the increased vulnerability of the aged macula to immune-related neurodegeneration. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Brain Structure and Function Springer Journals

Microglia in the primate macula: specializations in microglial distribution and morphology with retinal position and with aging

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Publisher
Springer Berlin Heidelberg
Copyright
Copyright © 2017 by Springer-Verlag Berlin Heidelberg (outside the USA)
Subject
Biomedicine; Neurosciences; Cell Biology; Neurology
ISSN
1863-2653
eISSN
1863-2661
D.O.I.
10.1007/s00429-017-1370-x
Publisher site
See Article on Publisher Site

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