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Hui Lu Faculty Member

My lab is interested in understanding the bidirectional link between physiological changes in neural circuitry and behaviors. We use the tools of in vivo two-photon calcium imaging, optogenetics, mouse genetics, computational analyses and machine learning approaches to characterize neural circuit coding of mouse behavior and understand the dysfunction of neural circuits in mouse models of human diseases. My fascination with the brain began when I was an undergraduate in biology major, and I foresaw that the approaches of computer science would be very valuable in studying brain function. Fortunately, my undergraduate performance was such that I was urged to enter the MS program in neuroscience without having to take the entrance exam; I took advantage of this offer to build a foundation in neuroscience while planning where to apply in the U.S. for graduate school. I was accepted into the Neuroscience program at UC Berkeley in 2004, where I joined the laboratory of Mu-ming Poo, PhD to learn electrophysiological, biochemical, and imaging methods as I studied the molecular mechanisms of cocaine addiction. I then joined the laboratory of Yang Dan, PhD as a postdoctoral fellow to learn how to apply in vivo functional imaging techniques to settling a long-standing question in the development of visual cortical circuit. To gain experience in studying neurological diseases, I joined the laboratory of Huda Y. Zoghbi, MD at Baylor College of Medicine for a second postdoctoral fellowship. There I applied the imaging and electrophysiological techniques I had learned to explore the neural circuit dysfunctions in two neurodevelopmental diseases related to dysfunction of the X-linked gene MECP2 (Rett syndrome and MECP2 duplication syndrome. Using two-photon calcium imaging on CA1 pyramidal cells in hippocampal slices, I found that loss and gain of MeCP2 function both lead to the same hippocampal circuit abnormalities, despite nearly opposite transcriptional profiles; moreover, I showed that this circuit dysfunction could be rescued by deep brain stimulation in a Rett syndrome mouse model. While in the Zoghbi lab I also contributed to projects on other neurodevelopmental disorders, such as those involving SHANK3, and to studies of MeCP2 effects in GABAergic and glutamatergic neurons. Now, in my independent lab at GWU, we have pursued deeper analyses of circuit dysfunctions in MeCP2-deficient mice, as related to motor function, social interactions, and emotional states.

Research Areas

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