Assitant Professor, Dept. of Basic Medical Sciences
University of Arizona College of Medicine Phoenix, USA
Dr. Shenfeng Qiu was trained in Medicine in China (M.D., 1994; M.P.H., 1997). He obtained his Ph.D. degree from University of California, Riverside, with his dissertation focusing on a neurotoxin (domoic acid). His Ph.D. thesis work has uncovered novel sequelae resulting from lower levels of domoic acid exposure to the nervous system (neurotoxicity), which include changes of glutamate receptors developmental expression profiles, altered CaMKII autophosporylation, differential phosphorylation of glutamate receptor subunit GluA1, and disrupted long-term potentiation. Dr. Shenfeng Qiu completed his postdoctoral trainings at Vanderbilt and University of Southern California, with research efforts focusing on genetic/environmental determinants of brain development. Research in his lab at University of Arizona focuses on translating genetic risk factors for neurodevelopmental/neuropsychiatric disorders into underlying mechanisms at molecular, cellular and neural circuit levels, with the expectation that revelation of these novel mechanisms will guide future therapeutic and developmental interventions for these disorders.
The overall interest of Dr. Shenfeng Qiu's laboratory is to understand brain origins of neurodevelopmental and neuropsychiatric disorders, such as autism spectrum disorders (ASD) and Schizophrenia. To achieve this goal, the lab utilizes mouse models developed for these disorders and explores the aberrant organization and function of cortical microcircuits that may relate to disease etiology. One project currently funded by NIH involves studying the role of MET protein tyrosine kinase. MET protein and its ligand hepatocyte growth factor (HGF) are transiently expressed in the developing brain across many species. However, the role of this signaling system in brain development remains largely unknown. Human genetic works have identified MET as a major risk gene for autism spectrum disorders, a collection of childhood diseases of neurodevelopmental origin. The overall goal of this project is to identify the mechanisms by which MET signaling affect neuronal growth and functional maturation. This research objective is approached at molecular, cellular and system levels using experimental mouse models. The mechanistic insights gained from studying mice may be extrapolated to humans. Thus a better understanding of MET-mediated signaling in brain development may lead to novel approaches on behavioral and developmental interventions that could improve the outcomes of ASD and potentially other neurodevelopmental disorders. To achieve our research goals, we are taking the advantages of in vivo and in vitro preparations of mouse brain tissues to examine the neuronal signaling in both normal animals and clinical models of neurodevelopmental disorders. We approach our questions by using a myriad of neuroscience techniques including morphological (histology, biocytin labeling, Golgi impregnation), functional (hippocampal slice field potential recording; patch clamp whole cell recording; laser scanning photostimulation for local circuit mapping; the developing optogenetic approaches of long-range circuit mapping), and molecular genetics (biochemistry and molecular biology experiments; siRNA mediated antisense knockdown; next generation sequencing/RNAseq, genetic mouse lines modeling human disorders).