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The Levinson Emerging Scholars Program

Lauren Hanson - Neurobiology & Public Health

Lauren Hanson. 2008 WRFF and Levinson ScholarGrowing up the daughter of two physical therapists instilled a passion for health and a curiosity about the human nervous system in me early on. When I began my first quarter at the University of Washington I had my sights set on pursuing a career in medicine but felt completely lost in how to successfully achieve that end. My intense desire to understand the intricacies of the correctly and incorrectly functioning human body inspired me to apply for entrance into the neurobiology program in my sophomore year. Early admittance into this program has allowed my neurobiology courses to serve as a foundation for my academic experience as an undergraduate. Through my neurobiology studies I found my true passion and have since forged what I know is the right path for me as an undergraduate. Following the first year of this program I actively sought a place in Dr. Moody’s lab knowing that his developmental neurobiology based research was something I wanted to pursue. My passion for the research I have been conducting over the past year and a half is driven both by my inquisitive nature and by the possible clinical applications my work may have for disorders in humans . An understanding of correct brain development has the potential to facilitate an understanding of later development when the mechanisms I study may contribute to pathological forms of brain activity such as seizures.

Mentor: Dr William Moody, Neurobiology

Project Title: Initiation Mechanisms of Spontaneous Synchronous Activity in Neonatal Mouse Cortex

Abstract: Spontaneous Synchronous Activity (SSA) plays a central role in mammalian nervous system development. In mouse cortex, SSA is vital for the development of neuronal characteristics necessary for normal information processing. For SSA to carry out its developmental functions and mature firing properties to emerge, it must begin and end within a critical temporal window. As such, how the timing and generation of SSA are controlled is a major question in neurobiology. The Moody lab has determined that a discrete pacemaker region in mouse cortex controls SSA. The question about pacemaker function has been approached from three different directions: multi-cell calcium imaging of neuronal activity, molecular studies of ion channel types, and direct electrophysiological recording from single neurons in living brain slices. My work thus far has used the technique of single-cell electrical recording, patch clamp, because it provides access to the most direct information about pacemaker mechanisms via single cell behaviors and responses. A likely candidate for a pacemaker current is the low-threshold inactivating (T-type) Ca2+ current so we have investigated the role this current plays in SSA using the three previously mentioned experimental approaches. Molecular studies of ion channels have shown that the T-type Ca2+ channel protein is highly concentrated in the ventro-lateral pacemaker region which matches the point of origin of SSA waves detected in our multi-cell calcium imaging experiments. Additionally, imaging experiments have shown that Mibefradil, a T-type Ca2+ blocker, blocks SSA. My previous patch clamp recording analysis comparing pacemaker and follower neurons shows significantly longer burst durations in pacemaker neurons, which is consistent with the presence of T-type Ca2+ currents. From these findings my future experiments will attempt to further elucidate the mechanisms of pacemaker initiation of SSA in mouse cortex using single-cell electrical recording to isolate the T-type Ca2+ current in voltage clamp recordings. I will also investigate the effects of Mibefradil on SSA in single cells in the pacemaker and follower regions and determine if the pacemaker quality of the initiation zone is a function of a network property or individual pacemaker qualities of the discrete component cells.