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Vision Training Seminar

Friday, December 08, 2017,

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  • Location: Langford Auditorium TN
  • Room: Langford-MRB IV, Room 11455

Kacie Dougherty

Ocular dominance across the layers of V1 in the awake behaving primate

Our brains take the input to the two eyes and combine those inputs in a way that leads to a singular view of our visual world. A full understanding of the neuronal basis of this binocular combination is not known, yet important for clinical treatment of binocular vision disorders. Almost all of the neurons in the lateral geniculate nucleus (LGN) are driven by stimulation of one eye only. In primary visual cortex (V1), the next stage in the primary visual pathway, most neurons respond to either eye, with one eye often evoking stronger responses than the other (ocular dominance). In this study, we examine ocular dominance across the layers of V1 by taking advantage of linear multi-contact electrode arrays. After training two macaques to fixate on a computer screen, we presented sine-wave gratings to one eye or the other eye, and simultaneously recorded local field potentials (LFP), single- and multi-unit spiking across the layers of V1. To estimate the thalamic input to layer 4C, we converted the LFP into laminar current source density (CSD), a measure of net synaptic excitation. Congruent with idea that they reflect LGN input, CSD responses in layer 4C showed strong ocular dominance. In our single-unit population, the large majority of neurons responded to stimuli presented to either eye, with the exception of a very small fraction of completely monocular neurons in layer 4C. Across the layers, layer 4C and layer 2/3 presented the most monocular spiking responses. These results show a non-uniform profile of ocular dominance across the layers of V1 and reveal that strong ocular dominance is not exclusive to the primary thalamic input layer.

Melissa Cooper and David Calkins

Astrocytes Redistribute Metabolic Resources to Compensate for Glaucomatous Stress

Optic nerve astrocytes provide support for retinal ganglion cell (RGC) axons, which transmit retinal signals to the brain. In glaucoma, a neurodegenerative disease affecting 80 million people, sensitivity to intraocular pressure (IOP) challenges RGC axons early. We find that mitochondrial density within the nerve diminishes after IOP exposure, perhaps due to early loss of anterograde transport function. Concurrently, astrocyte processes remodel in a predictable, quantifiable pattern. Each of these events presage overt axonal degeneration. Importantly, astrocytes have the unique ability to create glycogen, the brain’s largest energy reserve. In microbead occlusion model of glaucoma, glycogen stores diminish with IOP elevation in both the microbead and contralateral saline nerve. Using positron emission tomography we find that after microbead occlusion, glucose, the product of glycogen breakdown, redistributes from healthy to diseased optic nerve. Thus, astrocyte reorganization in the optic nerve may compensate for stressors that occur early in neurodegeneration in glaucoma.