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Arturo Ortin-Martinez, Diego García-Ayuso, F Javier Valiente-Soriano, Manuel Jímenez-López, María P. Villegas-Pérez, Marta Agudo-Barriuso, Pete Coffey, Anthony A. Vugler, Manuel Vidal-Sanz, Ma'ayam Semo; Population Of Melanopsin-expressing Retinal Ganglion Cells In Aging Wildtype And Rodless/coneless Mice: A Detailed Quantitative And Topographical Analysis. Invest. Ophthalmol. Vis. Sci. 2011;52(14):3466.
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Outer retinal degeneration in the rd/rd mouse model leads to retinal ganglion cell loss (at ~1 yr of age). However old mice (>2 yrs) lacking both rods and cones (rd/rd cl) and wildtypes maintain melanopsin-mediated responses to light. The density of melanopsin cells declines with advanced age in both wildtypes and rd/rd cl independently of retinal degeneration. Here we analyse the total numbers and the distribution of intrinsically photosensitive melanopsin positive ganglion cells in the retina during advanced aging (1-2.5 years) in wildtype mice and compare it to aging congenic rd/rd cl mice.
Mice were sacrificed at 1, 1.5 and 2.5 yrs of age (n=3-4 per group), retinae dissected as flatmounts, and melanopsin detected with immuno-fluorescence, some retinae were also co-labelled with a general ganglion cell marker Brn3a. Detailed maps of the retina were obtained using a Zeiss LSM 710 confocal microscope and the whole population of melanopsin positive cells was quantified.
Melanopsin cells were found distributed across the retinae at all ages and in all genotypes and were not found to be Brn3a positive. At 1 yr the wildtypes and rd/rd cl have similar total numbers of melanopsin cells, however by 1.5 yrs the rd/rd cl has fewer cells in comparison to age-matched wildtypes (P<0.05). By 2.5 yrs the wildtypes have fewer melanopsin cells than they did at 1 yr with counts at a similar level to the rd/rd cl at 1.5 yrs.
Outer retinal degeneration causes the melanopsin cell population to decrease at a faster rate however advanced aging in the wildtype leads to a similar loss of melanopsin positive cells. The maintenance of relatively un-attenuated irradiance detection responses into old age despite this reduction suggests there may be some compensatory plasticity enhancing signaling of the melanopsin system in old age.
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