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Vanderbilt Vision Training Seminar

Friday, January 11, 2019,
  • Location: Vanderbilt Eye Institute (VEI) • 2311 Pierce Ave. • Nashville , TN 37232
  • Room: Elliott Conference Room

Sarah Naguib

Vanderbilt Brain Institute (Rex Lab)

Vanderbilt University

“Galantamine confers neuroprotection from ocular trauma”

 Purpose: Our goal was to investigate the neuroprotective effects of galantamine, an FDA-approved mild Alzheimer’s Disease treatment, in a mouse model of blast-induced traumatic optic neuropathy.

 Methods: We exposed one eye of an anesthetized mouse to two bursts of over-pressurized air, 0.5 seconds apart for three days in a row. Blast and sham mice were given either regular or galantamine water (120mg/L) ad libitum, beginning immediately after blast and continuing for one month following blast. Optic nerves and retinas were collected at one-month after injury. Electrophysiology and optical coherence tomography were performed prior to collection. Optic nerve and retina histology, ELISAs, TUNEL, and immunohistochemistry were performed to assess activation of sterile inflammation, cell death, and synaptic changes.

 Results: Galantamine treatment preserved retina thickness and visual function. Since galantamine is known to affect ACh neurotransmission we assessed for changes in synaptic connections. Galantamine preserved synaptic connectivity based on immunolabeling of synaptophysin, a marker of the ribbon synapse, and calbindin-D, a marker for horizontal cells, or PKCa, bipolar cells. Galantamine also prevented axon degeneration in the optic nerve.

Conclusion: The data suggests that treatment with galantamine after injury is effective in maintaining synaptic connectivity in the retina and preserving optic nerve axons and vision. Galantamine may be a promising treatment for indirect traumatic optic neuropathy.

Jacob Westerberg

Department of Psychology (Maier Lab)

Vanderbilt University

“Tracing Neural Signatures of Priming in Visual Search”

By repetitively performing many tasks, both simple and complex, you improve. A common example of this you may perform daily is the identification of traffic signs so that you have a safe commute. We want to understand how the brain becomes better at rapidly and accurately identifies important items in your environment with repetition. To do this we use a paradigm known as priming of pop-out visual search. In this task a participant repetitively identifies a conspicuous singleton item in an array of distractor items across several trials. This is commonly done by having the participant identify a red item among green distractors. After a block of trials searching for the same red stimulus, the feature swaps and participants now search for a green target among red distractors. Behavioral performance in this task shows that repetitively searching for the same color lowers response times and improves accuracy, and following a switch, the behavior ‘resets’. By having monkeys perform this task and recording neural activity at multiple scales, we can investigate how the visual system adapts to perform this task better with repetition in blocks and begin to trace where in the brain this occurs. In this talk I will discuss two experiments designed to investigate this question. The first aimed to determine whether a neural phenomenon known as performance monitoring contributed to the behavioral changes observed with priming. We found that while individual neurons in the Supplementary Eye Field, an area known to contribute to performance monitoring in visual search, did not modulate with visual priming, an Event-Related Potential indexing performance monitoring, measured extracranially, did modulate. This suggests performance monitoring may play a role in priming, but the properties of the Supplementary Eye Field are not sufficient to support it. The second, and currently ongoing, experiment aims to determine how visual attention impacts priming. By investigating two areas, the Frontal Eye Field and area V4, we can begin to understand how visual attention might modulate with priming.