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B. Trexler, A. Petrides; Demonstration of a Lack of Tracer Coupling Between AII Amacrines and a Population of ON Cone Bipolar Cells . Invest. Ophthalmol. Vis. Sci. 2006;47(13):2283.
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In the rod – AII pathway, rod signals pass from AII amacrine cells to ON cone bipolar cells via gap junctions. Recent evidence has suggested that some ganglion cells do not receive rod signals via this pathway (Volgyi et al. 2005. J. Neurosci. 24:11182–92). It follows that the ON cone bipolar cells that excite this population of ganglion cells must not receive rod inputs via the rod–AII pathway. Therefore, we sought to determine if there are any ON cone bipolars that are not coupled to AII amacrine cells.
We injected neurobiotin into several AII amacrine cells in whole mount rabbit retina, forming a ring of injected cells. We stained the retina with antibodies to Gα0 and PKCα as well as streptavidin to visualize the neurobiotin. Gα0 labels all depolarizing bipolar cells and PKCα labels all rod bipolar cells.
Within the interior of the ring of injected AIIs, we expect that the neurobiotin concentration is "saturated". In other words, the individual fluxes of neurobiotin from each injected AII should sum, and all cells that are coupled to each other should be labeled. Any cells that do not have neurobiotin are presumed to be uncoupled from the AII–ON cone bipolar network. ON cone bipolars were marked as Gα0 positive / PKCα negative. Our data show that there is a population of Gα0 + / PKCα – cells in the interior of the injected AII ring that do not stain for neurobiotin.
It appears that there is a population of ON cone bipolar cells that are not tracer coupled to AII amacrine cells, and therefore, they and the ganglion cells they excite would not receive input via the rod–AII pathway.
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