Upcoming Events

December 1, 2021
3:00 p.m., Rm 2-6408, K207 Auditorium @ Med Center, Plus Zoom Capability

CVS Research Talk: Juliette McGregor, Flaum Eye Institute, University of Rochester
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Restoring vision at the fovea

Currently little can be done to restore high quality vision to patients with retinal degeneration. Tasks like recognizing faces require high acuity vision which is mediated by the fovea, a specialized retinal structure unique to humans and non-human primates. Signals from the fovea dominate visual cortex and optimizing vision restoration therapies at this retinal location has the potential to yield higher quality outcomes. Adaptive Optics Ophthalmoscopy provides an innovative preclinical development platform for evaluating therapies in non-human primates, allowing cellular scale functional recording of restored responses from foveal retinal ganglion cells in the living eye. I will describe success using calcium imaging in the living eye to demonstrate optogenetic restoration of RGC activity in primate fovea and efforts to accelerate progress toward more naturalistic restored vision, using stem cell-derived photoreceptor replacement therapy. Key to the success of all of vision restoration therapies is understanding the impact of periods of long term vision loss on the retina and I will share recent data examining changes in foveal RGCs in the weeks and months following deafferentation. Finally I will consider the unique perceptual challenges which may arise when restoring light sensitivity to foveal tissue.

December 3, 2021
2:00 p.m., Zoom meeting

CVS Journal Club
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Discussion of paper by Boynton Colloquium speaker Ziad Hafed, led by Sanjana Kapisthalam

December 6, 2021
12:00 p.m., 269 Meliora Hall on the River Campus, Plus Zoom Capability

CVS Research Talk: Michael Telias, Flaum Eye Institute, University of Rochester
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The role of inner retinal remodeling in vision

In degenerative blinding diseases, such as retinitis pigmentosa and age-related macular degeneration, the death of the photoreceptors in the outer retina triggers pathophysiological changes in the surviving inner retina, collectively known as remodeling. These changes include abnormal gene expression, spontaneous neuronal hyperactivity, membrane hyperpermeability and ectopic de-novo neuritogenesis. Remodeling results in the corruption of receptive fields, breaking down retinal circuits that are essential for high-acuity vision. We have found that chronic hyperactivation of retinoic acid receptor (RAR) in retinal ganglion cells (RGCs) is responsible for many aspects of remodeling in the degenerating mouse retina. Moreover, our data suggests that RAR, a nuclear transcription enhancer, signals through purinergic-activated (P2X7) and cyclic nucleotide-gated (HCN) channels in the cell membrane, exerting cell-specific effects in Off-RGCs. Blockade of RAR or P2X7 reverses remodeling, resulting in reduced hyperactivity, enhanced signal-to-noise ratio and improvement of retinal responses to light initiated by surviving cones. Systemic treatment of late degeneration rd10 mice with the FDA-approved drug disulfiram rescues image-forming vision, opening the possibility of ‘anti-remodeling treatments’ as a novel approach to improve and restore vision in blinding disorders.

December 8, 2021
10:00 a.m., Zoom Webinar (Register online)

CVS Boynton Colloquium: Ziad Hafed, Centre for Integrative Neuroscience
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Unraveling the neural mechanisms of perceptual saccadic suppression

Visual sensitivity, probed through perceptual detectability of sudden stimulus onsets, is strongly impaired around the time of saccades. This robust perceptual phenomenon exhibits intriguing stimulus selectivity properties, which have previously been interpreted as reflecting active suppressive signals directly derived from the eye movement commands. However, the neural mechanisms underlying these selective properties have remained elusive. In my talk, I will describe neurophysiological and behavioral experiments that strongly recast interpretations of perceptual saccadic suppression mechanisms. First, using neurophysiology in awake monkeys, and their concomitant behavior, I will describe how different cell types within the same sensory-motor structure can actually exhibit differential forms of saccade-induced suppression. Thus, some neuron types violate the selective properties of suppression that are so robust in perception. I will then move to identifying a retinal origin of perceptual saccadic suppression, using ex-vivo retinal ganglion cell neurophysiology. Remarkably, the visual dependencies of retinal suppression (in ex-vivo mouse, pig, and monkey retinae) are the same as the perceptual dependencies reported by human observers seeing similar image sequences, with or without eye movements. I will finally end by showing how this insight, of a primarily visual origin of perceptual saccadic suppression, allows demonstrating that the classic stimulus selective properties of suppression can be easily violated with simple visual manipulations, thus potentially explaining the earlier monkey results alluded to above. This line of work demonstrates that perceptual saccadic suppression may not be saccadic at all, but instead reflects visual-visual interactions jumpstarted at the very first stage of visual processing in the brain.

December 15, 2021
3:00 p.m., Rm 2-6408, K207 Auditorium @ Med Center, Plus Zoom Capability

CVS Research Talk: Collynn Woeller, Flaum Eye Institute, University of Rochester
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April 6, 2022
3:00 p.m., Rm 2-6408, K207 Auditorium at URMC

CVS Boynton Colloquium: Christine Wildsoet, UC Berkeley, School of Optometry
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