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The Levinson Emerging Scholars Program

Mark Shi - Neurobiology and Biochemistry

Mark ShiWhen Mark Shi first came to the University of Washington, he was unsure of what he wanted to study and pursue as a career. That all changed while he was taking introductory biology, where he became fascinated with the intricate, behind-the-scene mechanisms that mediate our daily lives. Mark pursued this interest by joining the neurobiology program, where he had the opportunity to learn about one of the most complex and least understood systems of the human body. After his first year in the program, Mark began working in Dr. Bosma’s developmental neurobiology lab. This research has allowed Mark to expand on his knowledge of the nervous system by investigating new questions in the field. After graduating this year, Mark plans on continuing his research in Dr. Bosma’s lab while applying for medical school. He hopes to further develop his investigative research skills with the support of the Levinson Scholarship as he pursues a career as a physician.

Mentor: Martha Bosma, Biology

Project Title: Activity-Dependent Regulation of 5HT-Postitive Raphe Neurons in Developing Mouse Hindbrain

Abstract: In many regions of the developing nervous system, spontaneous synchronous activity (SSA) plays a role in synaptogenesis, cell positioning, ion channel development, and neuronal migration. SSA has been observed in the hindbrain, the most caudal of the three primary divisions of the developing vertebrate brain that develops into the cerebellum, pons, and medulla. These regions coordinate complex muscular movements, equilibrium, and autonomic functions. In previous studies, our lab has identified an internal pacemaker, which drives SSA during a discrete window of time during embryonic development; this pacemaker region is a cluster of serotonergic (5-HT) neurons located between rhombomeres (r) 2 and 3. We are currently examining the mechanism by which SSA develops in the hindbrain. Using intracellular calcium imaging to visualize electrical events, we have observed SSA primarily propagating rostro-caudally along the midline of hindbrains at embryonic day (E) 11.5. Culturing hindbrain tissue from E10.5 to E11.5 has allowed us to pinpoint requirements for SSA in vitro. We have shown that hindbrains cultured in the presence of ketanserin, a blocker of the 5-HT2 receptor, have SSA with reduced frequency at E11.5, and fewer 5-HT-positive neurons, as shown with immunocytochemistry. Tissues cultured in high concentrations of extracellular potassium or Valproic Acid (VPA), the latter of which is a model for autism in mice, exhibit an increased frequency in SSA. Furthermore, tissues cultured with VPA have SSA with greater amplitude that extends beyond the midline to lateral regions. We therefore postulate in this model of cultured hindbrain that activity itself is able to regulate the appearance and excitability of the cluster of 5HT-positive pacemakers that drive SSA in the hindbrain.