David Stoppel, Ph.D.
My research is focused on uncovering the neurodevelopmental mechanisms underlying visual cortical hyperexcitability in fragile-X syndrome. Throughout my career, my motivating research interest has been to understand how genetic or functional perturbations impact nervous system development. During graduate school, I generated transgenic mice which I used to identify populations of glutamatergic neurons in the ventral tegmental area that are disrupted in a mouse model of 15q11-13 duplication syndrome (dup15) and critical for regulating social behavior (Krishnan, Stoppel, and Nong et al., (2017) Nature 543(7646). Early in my postdoctoral training, I continued my work on dup15 and identified a population of molecularly defined neurons in the ventromedial hypothalamus that are dysregulated, resulting in increased aggression, a common and problematic comorbid feature of the disorder. Most recently at MIT, I have studied how the loss of Fmr1, the gene that causes fragile-X syndrome, alters the electrophysiological properties of layer V visual cortical neurons. I am currently working to identify the molecular mechanisms that underlie the excitability deficits in layer V neurons with the hope of uncovering novel therapeutic targets for the treatment of fragile-X syndrome.
Ph.D. in Neuroscience – Harvard University – 2014
B.Sc. in Neural Science – New York University – 2006