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Physics SPS Seminar Series

DATE:Tuesday, November 15, 2016
TIME: 12:30 PM - 1:30 PM
PLACE: MONROE HALL ROOM 152
SPEAKER: Dave Vumbaco, The Neuroscience Center of Excellence, LSUHSC

 

A Primer on the Physics of Neuroscience and Studying Central Congenital Deafness.

The seminar will be given two parts. In the first part we will discuss the connections between physics and neuroscience. The abstract for the second part is as follows:

Usher syndrome (Usher) is the most common genetic disease causing combined deafness and blindness. The c.216G>A mutation (216A) in the USH1C gene, which is responsible for type 1 Usher in Acadian populations, causes aberrant splicing that results in a frameshift and a truncated RNA and Harmonin protein. Mice homozygous for the 216A mutation (Ush1c216AA) are deaf, and have vestibular and visual dysfunctions, similar to patients. Treatment of Ush1c216AA mice with antisense oligonucleotides (ASOs) rescues hearing, balance, and vision. The organization of the central auditory structures associated with Usher is unknown. We hypothesize that there are anatomical changes in central auditory structures including the primary auditory cortex (A1) and the ventral medial geniculate nucleus (MGv) in Usher mice. To explore this hypothesis, Ush1c216AA and normal hearing littermates were injected with BDA conjugated to a red fluorophore (BDA-red) into the MGv, and in the right primary auditory cortex with BDA conjugated to a green fluorophore (BDA-green). The intersection of the neural projections from the right A1 and the left MGv into left A1 was quantified along the mediolateral and rostrocaudal axes. Preliminary results suggest that the neuroanatomical pathways are significantly different in Ush1c216AA mice compared with normal hearing littermates. The quantity of BDA-red fluorescence is greater in Ush1c216AA mice compared to littermate controls, suggesting that the MGv projection into ipsilateral left A1 is expanded. Quantification of the BDA-green shows a reduction in fluorescence in the rostral region of A1 and an increase in the caudal region of A1 compared to littermate controls, suggesting the disorganized commissural right A1 to left A1 projections. Taken together, these results show, for the first time, defects in the central ascending auditory pathway in addition to peripheral defects associated with Usher syndrome.

 

 

 

Pizzas & Drinks will be served. Please arrive 10 minutes early!              

 

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