Associate Professor of Pharmacology
Ph.D., Biological Sciences
Stanford University, 1995
My laboratory is
interested in elucidating the mechanism by which neurotrophins
regulate the formation, maintenance, and function of neural
circuits in the brain. Deficiencies in neurotrophins have been
linked to neurodegenerative diseases, obesity, mental
retardation, mood disorders, and other neurological disorders.
Neurotrophins are a family of small and secreted growth factors,
which include brain-derived neurotrophic factor (BDNF), nerve
growth factor, neurotrophin-3, and neurotrophin-4/5. My
laboratory uses a combination of mouse genetic, biochemical,
molecular, histological, and behavioral approaches to identify
the neural and molecular pathways mediating the diverse
functions of neurotrophins. We have discovered that BDNF
synthesized in dendrites controls activity-dependent
modifications of dendritic spines, which are the postsynaptic
sites for the vast majority of excitatory synapses. We have also
found that neurotrophins are required for the formation and
maintenance of the striatum. Their deficiencies likely
contribute to selective degeneration of striatal neurons in
Huntington's disease. Much of the current work in the laboratory
focuses on the regulation of dendritic BDNF synthesis and its
role in synaptic plasticity and learning, molecular mechanisms
underlying the development and maintenance of the striatum and
its relevance to Huntington's disease, molecular and neural
substrates underlying the effect of BDNF on body weight, and
development of therapeutic strategies for neurological disorders
using BDNF or its mimetics.
Waterhouse EG, An JJ, Baydyuk M, Liao GY, Zheng K, Xu B.
BDNF promotes differentiation and maturation of adult-born neurons through GABA-ergic transmission
Liao GY, An JJ, Gharami K, Waterhouse EG, Vanevski F, Jones KR, Xu B.
Dendritically targeted Bdnf mRNA is essential for energy balance and response to leptin.
Kaneko M, Xie Y, An JJ, Stryker MP, Xu B.
Dendritic BDNF synthesis is required for late-phase
spine maturation and recovery of cortical responses following sensory deprivation.
Zheng K, An JJ, Yang F, Xu W, Xu ZQ, Wu
J, Hokfelt TG, Fisahn A, Xu B, Lu B.
TrkB signaling in parvalbumin-positive
interneurons is critical for gamma-band network
synchronization in hippocampus. Proc Natl Acad
Sci U S A. 108(41):17201-6, 2011
Baydyuk M, Russell T, Liao GY, Zang K, An JJ, Reichardt
LF, Xu B.
TrkB receptor controls striatal formation by regulating
the number of newborn striatal neurons.
Proc Natl Acad Sci U S A.
Baydyuk M, Nguyen MT, Xu
Chronic deprivation of TrkB signaling leads to selective
late-onset nigrostriatal dopaminergic degeneration.
Xie Y, Hayden MR, Xu B.
BDNF Overexpression in the Forebrain Rescues
Huntington's Disease Phenotypes in YAC128 Mice.
Lau AG, Irier HA, Gu J,
Tian D, Ku L, Liu G, Xia M, Fritsch B, Zheng JQ,
Dingledine R, Xu B, Lu B, Feng Y.
differentially regulate activity-dependent translation
of brain-derived neurotrophic factor (BDNF).
Proc Natl Acad Sci U S A.
Fu X, Zang K, Zhou Z,
Reichardt LF, Xu B.
signaling requires a protein interacting with receptor
tyrosine kinases via C2H2 zinc fingers.
Mol Biol Cell.
Waterhouse EG, Xu B.:
New insights into the role of brain-derived neurotrophic
factor in synaptic plasticity.
Cell Neurosci., 2009
An JJ, Gharami K, Liao GY, Woo NH, Lau AG, Vanevski F,
Torre ER, Jones KR, Feng Y, Lu B, Xu B.:
Distinct role of long 3' UTR BDNF mRNA in spine
morphology and synaptic plasticity in hippocampal
Cell. 134:175-87, 2008
Liao GY, Xu B.:
Cre recombinase-mediated gene deletion in layer 4 of
murine sensory cortical areas.
Genesis. 46:289-93, 2008
Gharami K, Xie Y, An JJ, Tonegawa S, Xu B.:
Brain-derived neurotrophic factor over-expression in the
forebrain ameliorates Huntington's disease phenotypes in
J Neurochem. 105:369-79, 2008
Xu B, Goulding EH, Zang K, Cepoi D, Cone RD, Jones KR,
Tecott LH, Reichardt LF.:
Brain-derived neurotrophic factor regulates energy
balance downstream of melanocortin-4 receptor.
Nat Neurosci. 6:736-42, 2003
Rico B, Xu B, Reichardt LF.:
TrkB receptor signaling is required for establishment of
GABAergic synapses in the cerebellum.
Nat Neurosci. 5:225-33, 2002
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