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Changes in morphology of retinal ganglion cells with eccentricity in retinal degeneration

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Abstract

Ganglion cells are the output neurons of the retina and are known to remodel during the subtle plasticity changes that occur following the death of photoreceptors in inherited retinal degeneration. We examine the influence of retinal eccentricity on anatomical remodelling and ganglion cell morphology well after photoreceptor loss. Rd1 mice that have a mutation in the β subunit of phosphodiesterase 6 were used as a model of retinal degeneration and gross remodelling events were examined by processing serial sections for immunocytochemistry. Retinal wholemounts from rd1-Thy1 and control Thy1 mice that contained a fluorescent protein labelling a subset of ganglion cells were processed for immunohistochemistry at 11 months of age. Ganglion cells were classified based on their soma size, dendritic field size and dendritic branching pattern and their dendritic fields were analysed for their length, area and quantity of branching points. Overall, more remodelling was found in the central compared with the peripheral retina. In addition, the size and complexity of A2, B1, C1 and D type ganglion cells located in the central region of the retina decreased. We propose that the changes in ganglion cell morphology are correlated with remodelling events in these regions and impact the function of retinal circuitry in the degenerated retina.

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Acknowledgments

The authors are grateful to Cameron Nowell for assistance in using metamorph software and to A/Prof Tony Hannan for donating the Thy1-YFP mice.

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Correspondence to E. L. Fletcher.

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This work was supported by an NHMRC project grant (APP1021042), by Retina Australia and by the Australian Research Council through its Special Research Initiative in Bionic Vision Science and Technology grant to Bionic Vision Australia.

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Anderson, E.E., Greferath, U. & Fletcher, E.L. Changes in morphology of retinal ganglion cells with eccentricity in retinal degeneration. Cell Tissue Res 364, 263–271 (2016). https://doi.org/10.1007/s00441-015-2337-y

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  • DOI: https://doi.org/10.1007/s00441-015-2337-y

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