Abstract
The AII amacrine cell, a unique rod signal integrator passing through the cone bipolar cell to ganglion cells, uses parvalbumin as a transducer of cytosolic calcium ion signals in the mammalian retina. For clarification of whether AII amacrine cell network contributes to the early neuropathogenesis of diabetic retinopathy, this study first analyzed alteration of parvalbumin expression in experimental diabetic retinas using immunohistochemical methods. Parvalbumin immunoreactivity was found in AII amacrine cells, some amacrine cells of a wide-field type, and displaced amacrine cells of the normal rat retina. During diabetes, cell density of each parvalbumin immunoreactive amacrine cell type showed no large changes despite decrease in immunoreactivity especially in AII amacrine cells. In addition to these parvalbumin immunoreactive amacrine cell types, a type of cone bipolar cells co-expressing glutamate transporter 1b and connecting electrically with AII amacrine cells appeared clearly by 4 weeks of diabetes, and thereafter sharply increased in number to that of AII amacrine cells. Protein levels of parvalbumin throughout the diabetic retinas also showed no large changes, except a transitional slight increase at 4 weeks of diabetes. These results suggest that the parvalbumin expression propagates from AII amacrine cells to a type of cone bipolar cell through electrical synapses due to dysfunction of biased mechanism in calcium ion buffering, caused by diabetic injury, and thus AII amacrine cells are closely involved in neuropathogenesis of ongoing diabetic retinopathy.
Published Version
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