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In this thesis, I use a range of techniques in computational neuroscience, communication theory, and electrophysiology to characterize functional changes that occur in early stages of retinal degeneration in the mouse. At post natal day 14, retinal ganglion cells in the rd1 mouse exhibit peculiar differences from age matched controls: an increased latency of responses to the onset of a light stimulus, decreased spike count in response to stimulus onset, increased spontaneous firing activity, and a decrease in information transmission. I propose this is due to an up-regulation of OFF bipolar cell excitation, a critical factor in functional changes seen in rd1, and use innovative techniques to discover findings that support these claims.