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Ning Tian, Tao He, Xavier Mortensen, Ping Wang; Dendritic reorganization of starburst amacrine cells secondary to retinal ganglion cell death. Invest. Ophthalmol. Vis. Sci. 2017;58(8):2596.
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© ARVO (1962-2015); The Authors (2016-present)
To quantify surviving and dendritic reorganization of starburst amacrine cells secondary to retinal ganglion cell (RGC) death due to optic nerve crush (ONC) and the possible role of CD3ζ mediated signals in the dendritic development and degeneration of starburst amacrine cells.
ONC was performed unilaterally in mice expressing YFP in starburst amacrine cells with or without mutation of a key component of T-cell receptor complex, CD3ζ. Cells in the ganglion cell layer (GCL) labeled by DAPI, ChAT-positive cells in both GCL (displaced starburst amacrine cell, DSAC) and inner nuclear layers (INL, conventionally located starburst amacrine cell, SAC) were quantified for cell density 7 or 10 days after ONC. Individual YFP-expressing starburst amacrine cells were imaged using confocal microscopy and their dendrites were quantified using Neurolucida software.
Dendritic architectures of SACs and DSACs are significantly different. The ONC procedure caused 31% cell loss in the GCL 10 days after ONC. However, SACs and DSACs lose their dendrites by 24% and 20% respectively without cell death. In CD3ζ mutants, the size of dendritic field of DSACs was increased by 38%, the dendritic length of SACs were decreased by 10% and the cell density was increased by 19%. However, mutation of CD3ζ has no significant effect on RGC death or dendritic reorganization of starburst amacrine cells after ONC.
RGC death caused by ONC is associated with immediate dendritic reorganization of starburst amacrine cells. CD3ζ regulates the development of dendritic architecture of starburst amacrine cells but not dendritic reorganization of these cells after RGC death.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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