The full or partial deafferentation of neural circuits is an inevitability in the life of an organism. The mature nervous system is thus tasked with maintaining a stable output in the face of lost input. Deafferentation has been studied in numerous sensory systems, but nowhere is the problem so well defined and controllable as in the visual system. Despite a deep literature on deafferentation in visual cortex, it remains unknown how the retina contributes to this plasticity. In this dissertation, I show that the mature retinal circuit compensates for input lost after half of either the cone or rod photoreceptors have been ablated. In Chapter 1, I demonstrate that after loss of half of the cone population, functional compensation arises via inhibitory currents onto ganglion cells. In Chapter 2, I demonstrate that after loss of half of the rod population, functional compensation arises via inhibitory currents onto rod bipolar cells. In both studies, I examine morphology and physiology and use partial stimulation of control retina to dissociate response properties resulting from decreased input and response properties resulting from subsequent plasticity within the circuit. In Chapter 3, I discuss principles that emerge from comparing these two studies and how these results may inform current efforts to develop diagnostic tools and therapies to restore vision.
|Advisor:||Dunn, Felice A|
|Commitee:||Stryker, Michael P, Copenhagen, David R, Horton, Jonathan C|
|School:||University of California, San Francisco|
|School Location:||United States -- California|
|Source:||DAI-B 81/4(E), Dissertation Abstracts International|
|Keywords:||Deafferentation, Ganglion cells, Inhibition, Plasticity, Retina, Vision|
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