SEMINARS

Seminar: From dendrites to behavior: Circuit mechanisms of active sensation in the neocortex.

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Seminar: Imaging brain structure and function in health and disease

**Speaker: Dr. Timothy H. Murphy, University of British Columbia **Time: Feb 27, 2013, 3:30-5:00 pm **Place: Administration Building, Room 502 **Host by: Prof. Shumin Duan **Speaker Brief Introduction: Timothy H. Murphy, BSc, PhD Affiliation Professor, Departments of Psychiatry and Cellular and Physiological Sciences, University of British Columbia, Vancouver, British Columbia, Canada. Dr. Murphy is a basic scientist who applies high-resolution imaging techniques to questions involving stroke in live animals. Currently the laboratory is employing a variety of complimentary imaging modalities which permit resolution of individual synapses within living mice using 2-photon microscopy to regional imaging techniques which allow monitoring of brain function or blood flow. Dr. Murphy’s past teaching experience in microscopy methods includes an instructorship in the Cold Spring Harbor laboratories Imaging Neurons course, as well as the University of British Columbia 3D microscopy course. The aim of Dr. Murphy’s work is to understand the neurochemical and structural changes that occur to brain circuitry during the first few hours following an ischemic event as well as recovery over weeks to months. By combining high resolution structural imaging in live mice with the ability to do somatosensory response mapping, Dr. Murphy’s has evaluated relationships between synaptic structure and brain circuit function. His lab currently employs 2-photon microscopy for submicron resolution of synaptic elements in live brain tissues. The lab is also actively engaged in developing methods for mapping the mouse brain before and after stroke that employ light-activated ion channels such as channelrhodopsin-2. Knowledge from these imaging experiments could lead to new means of human therapeutics involving brain stimulation or recommendations concerning stroke treatment or rehabilitation. Publications: Dr. Murphy has very productive publications in high-impact journals, includingScience, Nature Neuroscience, Nature Method, Nature reviews, Neuron, PNAS, J Neuroscience, Stroke, JBC, JCBFM, JP, etc (highlighted publications)

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Seminar: Dr. Qidong Hu（UCSD）; Dr. Zhihong Zhou（UCSD）

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Seminar: In Sights into Human Aging Based on Pluripotent Stem Cells and Gene Target Modification

**Speaker: Guanghui Liu, PhD **Time: Jan 17, 2013, 2:30 pm **Place: Research Building, Room B502, School of Medicine **Speaker Brief Introduction: Guanghui Liu, PhD Professor, Institute of Biophysics, Chinese Academy of Sciences Education and Research Experience 1997-2002，B.S., Peking University Health Science Center 2002-2007，Ph.D., Institute of Biophysics, Chinese Academy of Sciences 2007-2009，Research associate, Dept. of Cell and Molecular Biology, The Scripps Research Institute 2009-2011，Research associate, Gene expression laboratory, The Salk Institute for Biological Studies 2010-2011，CIRM scholar, California Institute of Regenerative Medicine (CIRM) 2011-，Glenn fellow, Glenn Aging Foundation 2011-，Professor, Institute of Biophysics, Chinese Academy of Sciences 2012，Thousand Young Talents program of China Research Interests 1. Modeling human diseases with pluripotent stem cells (PSCs) 2. Editing human genome in hPSCs 3. Mechanism of human aging and longevity 4. Nuclear architecture, chromatin organization, and human diseases Representative publications (1equal contribution; *Corresponding author) 1.Liu GH1*, Qu J1, Suzuki K1, Nivet E, Li M, Montserrat N, Yi F, Xu X, Ruiz S, Zhang W, Ren B, Wagner U, Kim A, Li Y, Goebl A, Kim J, Soligalla R, Dubova I, Thompson J, Yates J III, Esteban C, Sancho-Martinez I, Belmonte JC*. Progressive degeneration of human neural stem cells caused by pathogenic LRRK2.Nature. 2012; 491(7425):603-7. 2. Pan H1, Cai N1, Li M, Liu GH*, Izpisua Belmonte JC*. Autophagic control of cell stemness. EMBO Mol. Med. 2013. In press 3. Liu GH1*, Ding Z1, Izpisua Belmonte JC*. iPSC technology to study human aging and aging-related disorders.Curr Opin Cell Biol. 2012; Dec;24(6):765-74 4. Li M1, Liu GH1, Belmonte JC.Navigating the epigenetic landscape of pluripotent stem cells.Nat Rev Mol Cell Biol.2012; 13(8):524-35. 5. Liu GH1, Suzuki K1, Qu J1, Sancho-Martinez I, Yi F, Li M, Kumar S, Nivet E, Kim J, Soligalla RD, Dubova I, Goebl A, Plongthongkum N, Fung HL, Zhang K, Loring J,Laurent L, and Belmonte JC. Targeted gene correction of laminopathy-associated LMNA mutations in patient-specific iPSCs. Cell Stem Cell. 2011; 8(6):688-94 6.Liu GH, Barkho BZ, Ruiz S, Diep D, Qu J, Yang SL, Panopoulos AD, Suzuki K, Kurian L, Walsh C, Thompson J, Boue S, Fung HL, Sancho-Martinez I, Zhang K, III JY, Belmonte JC. Recapitulation of premature ageing with iPSCs from Hutchinson-Gilford progeria syndrome. Nature. 2011; 14;472: 221-5

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Seminar: LAP protein Erbin regulates neuregulin signaling and neural developmen

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Seminar: Proton channel in the brain: pH regulation and beyond

**Speaker: Dr. Long-Jun Wu, Rutgers University **Time: Jan 8, 2013, 10:00 am **Place: Research Building, Room B502, School of Medicine **Speaker Brief Introduction: Long-Jun Wu, Ph.D., Assistant Professor Department of Cell Biology and Neuroscience Rutgers University The long-term goal of Wu lab is to understand microglia-neuron communication in the brain. Microglia are the principal immune-response cells in the central nervous system. Resting microglia constantly survey the microenvironment in the normal brain. Upon brain dysfunction, microglia are activated and exert detrimental or beneficial effects on the surrounding neurons. Microglia have remarkably fast and dynamic activities in both the normal and pathological brain. An exciting possibility is that they are communicating with neurons through ion channel mechanisms. In neuronal circuits, microglia are assumed to be crucial to synaptic pruning and plasticity, yet no direct evidence has been identified. Microglia are strongly activated in pathological conditions such as pain, stroke and neurodegeneration, however, the molecular mechanisms for microglial activation and function in brain diseases are still controversial. Overall, they are interested in three interrelated topics on microglia-neuron communication: (1) The ion channel mechanism of microglia-neuron communication; (2) Microglia in synaptic function; and (3) Microglia’s contribution to neuropathic pain. We have been exploring microglia chemotaxis (Wu et al., Glia, 2007, Fig.1), microglia in synaptic plasticity (Wu and Zhuo, J Neurophysiol, 2008), as well as an unique microglial voltage-gated proton channel, Hv1, in the brain (Wu et al., Nat Neurosci, 2012). Taking Hv1 proton channel as an entry point, their initial project will study direct communication from microglia to neurons through microglial Hv1. They will then explore how microglia function in neuronal circuits under normal and pain conditions. The results from their studies would advance the understanding of microglia function in the brain and provide therapeutic targets for neuropathic pain treatment.

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Seminar: negative emotional vulnerability and its adaptive significance

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Seminar: Cellular polarity and tissue morphogenesis: the roles and mechanisms o

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Mini symposium: Brain Disorder and Translational Research

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Seminar: Application of AAV gene therapy Vectors; Application of TALEN

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