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Vanderbilt Vision Training Seminar

Friday, January 12, 2018,
  • Location: Vanderbilt Eye Institute (VEI) • 2311 Pierce Ave. • Nashville , TN 37232
  • Room: Elliot Conference Room

Rachel Fischer

Department of Pharmacology

Vanderbilt University

Altered potassium homeostasis in glaucoma and significance for retinal ganglion cell health

Retinal ganglion cell (RGC) degeneration is the cause of irreversible blindness for millions of individuals worldwide. Glaucomatous vision loss results from degeneration of RGC axons, which comprise the optic nerve. Glaucoma produces functional deficits in RGCs prior to structural degeneration. There is a potential therapeutic window after the onset of functional deficits, but prior to irreversible, physical loss of RGC axons in which axonopathy could be interrupted and further vision loss prevented. Our goal is to identify factors involved in the progression from functional deficits to structural RGC degeneration. Glaucoma patients experience vision loss in clusters across their visual field, rather than in a uniformed manner. Studies in animal models of glaucoma indicate that RGC axonopathy occurs in similar patterns. This suggests that external cues in the immediate milieu may play a role in propagating disease progression to neighboring RGCs. Early RGC axonopathy includes functional deficits in axon transport. Preliminary data from our lab indicates that RGC transport deficits are accompanied by electrophysiological impairments. One possible explanation for these electrophysiological impairments is a disruption in the K+ homeostasis in the retina. In RGCs, the Na/K-ATPase is responsible for re-establishing the electrochemical gradient of ions, in order to maintain proper K+ homeostasis in the retina. Our preliminary data indicates that there is a significant disruption in the K+ homeostasis in glaucomatous retina. We found changes in expression of the Na/K-ATPase in glaucomatous retina, as well as altered ion flux through K+ channels in cells subjected to glaucoma-related stressors. We are testing the central hypothesis that abnormal electrochemical gradients arising from electrophysiological impairment contribute to spatiotemporal progression of pathology between neighboring RGCs.

Jacob Westerberg

Department of Psychology

Vanderbilt University

Repetitive Stimulation Enhances V1 Encoding Efficiency 

Repeated stimulus presentations reduce neuronal responses across many brain areas (repetition suppression) while improving performance in associated tasks (repetition priming). The neuronal mechanisms that enhance performance in the face of reduced brain activity are unknown. Here we demonstrate that stimulus repetition increases encoding efficiency among cortical neurons, which enhances stimulus representations despite reduced spiking activity. Using a repetition priming-evoking stimulus sequence, we recorded laminar responses in monkey primary visual cortex (V1). We found that repetition suppression is most pronounced outside the V1 layers that receive retinogeniculate input and is robust to alternating stimuli between the two eyes, suggesting that repetition suppression is of cortical origin. This V1 spiking suppression is accompanied by sharpened neural tuning as well as increased neuronal synchrony, however not by decreased response latency. These results suggest that repetition priming and repetition suppression arise from modulated cortical neuronal processing that enhances encoding efficiency as stimuli repeat.