​Graduate Students Seminar

Seminar | March 5 | 12-1 p.m. | 489 Minor Hall

 Vasha Dutell, Bruno Olshausen Lab; Emilia Zin, John Flannery Lab

 Neuroscience Institute, Helen Wills

Vasha Dutell’s Talk Title: Natural Visual Signals and Heterogeneous Networks Optimized to Process Them

Abstract: One of the many mysteries of the retina is its great diversity of neuron types and subtypes. An example of this is the many retinal ganglion cells subtypes that independently tile visual space, creating multiple pathways that transmit different aspects of visual information to the brain in parallel. Given the constraints faced by the optic nerve, in particular a need for compression, encoding using separate populations appears somewhat puzzling. To shed light on this conundrum, we view the problem from an efficient coding standpoint, asking the question, ‘Are these parallel streams in the retina efficient strategies for encoding natural signals?’ To answer this question, we explore the statistics of the natural visual signal. First, we use static images, and discuss the On/Off cell split as an emergent property of a neural network model trained to compress natural images using few number of spikes per neuron. Finally, we extend this analysis into the time domain with movies, and discuss the magnocellular/parvocellular split as an efficient coding strategy for compressing natural video.

Emilia Zin’s Talk Title: AAV Mediated Rescue of Neuronal Ceroid Lipofuscinosis-Like Retinal Disease

Abstract: The several different types of neuronal ceroid lipofuscinosis (NCL) are the most common neurodegenerative diseases of childhood and can cause visual loss. NCLs can be caused by various gene mutations, and one of them, CLN11, is caused by mutations on the GRN gene. The deficiency of the protein coded by this gene, progranulin, leads to neuronal death both in the brain and retina at least in part owing to failure of nerve cells’ waste disposal system (the endolysosome). Most of the genetic defects that cause NCL is the consequence of similar endolysosomal dysfunction. Unlike other neurodegenerative diseases in which degeneration seems to be triggered by overexpression or abnormal production of a normal protein, CLN11 results from low levels of progranulin protein. Therefore, restoring or enhancing progranulin via a gene therapy based approach represents an attractive target for treating CLN11. An adeno-associated virus (AAV) capsid that can infect all layers of the retina (7m8) may target all retinal neurons with a healthy copy of the GRN gene in a GRN-/- mouse line. Furthermore, AAV serotype 9 (AAV9) is capable of passing through the developing blood-brain and blood-retina barriers in young mice, serving as a vector for GRN in mouse pups to target the retina and brain before degeneration begins. This approach allows us to determine the time dependency of both optimal and potential effectiveness of such gene delivery.