![]() ![]() 003548 The Jackson Laboratory, Bar Harbor, ME) were maintained in a pathogen-free colony by continuous mating with C57BL/6J (no. These abnormalities may explain some of the early anomalies in visual function induced by diabetes. The data show that retinal ganglion cells are lost from the peripheral retina of mice within the first 3 months of diabetes and that the dendrites of surviving large ON-type cells undergo morphologic changes. Abnormal swelling on somas, axons, and dendrites were noted in all subtypes of ganglion cells including those expressing melanopsin.Ĭonclusions. ![]() The structure of dendrites of ON-type retinal ganglion cells was affected by diabetes, having 32.4% more dendritic terminals ( P < 0.05), 18.6% increase in total dendrite length ( P < 0.05), and 15.3% greater dendritic density compared with control retinas, measured by Scholl analysis. Six different morphologic clusters of cells were identified in the mouse retinas. Thy1-YFP expression occurred throughout the entire structure of a smaller number of cells, including their soma, axons, and dendrites. There was a 16.4% reduction in the density of CFP-positive ganglion cells in the peripheral retina of Ins2 Akita/+ mice compared with wild-type control retinas ( P < 0.017), but no significant change in the central retina. Thy1-CFP expression was limited to retinal ganglion cell bodies. The morphology of surviving cells was examined, and dendritic density was quantified in Ins2 Akita/+ Thy1-YFP mice by using the Sholl analysis. The number of CFP-positive retinal ganglion cells was quantified in retinas of Ins2 Akita/+ Thy1-CFP mice. After 3 months of diabetes, the number and morphology of retinal ganglion cells was analyzed by confocal microscopy. Mice that expressed cyan fluorescent protein (CFP) or yellow fluorescent protein (YFP) reporter genes under the transcriptional control of the Thy1 promoter were crossed with Ins2 Akita/+ mice. To determine the extent of retinal ganglion cell loss and morphologic abnormalities in surviving ganglion cells in Ins2 Akita/+ diabetic mice.
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