The lab is interested in understanding the regulation of synaptic strength and synaptic mechanisms underlying neuronal circuit function in animal behavior. We believe that these research will provide fundamental insights into neural underpinnings for learning and memory, and will identify synaptic and neural circuit malfunctions that are involved in many neurological and mental disorders, such as Alzheimer's disease, depression and autism disorders. During the fiscal year, We have succeeded in setting up the lab for these research programs. This includes setting up three dual whole cell patch-clamp systems in the lab to perform electrophysiological analysis of neuronal activity, which are the essential component of the labs research program;setting up molecular, biochemical, imaging and histological equipment and reagents in the lab to facilitate scientific discoveries;setting up the equipment and methods for in vivo manipulations of gene expression in rodents (stereotaxic viral or drug injection, in utero cDNA electroporation and p0 newborn pup viral injection), which will provide important research tools to manipulate neuronal genes in vivo;and setting up the room and equipment for behavioral testing on rodent animals, which will allow us to test functional significance of manipulation of neuronal gene expression at systems levels. In addition, we have imported, maintained, expanded and created over twenty lines of transgenic and knockout mice in the lab, which laid the foundation for various research programs in the future. In parallel, we have developed two animal protocols that have been approved to initiate scientific research with these animals. Furthermore, we have recruited three scientists to join the lab to form a dynamic and motivated research team. This includes one research assistant and two postdoctoral fellows. On the research side, we have collected some promising preliminary data that indicate an important role for a novel protein in the regulation of excitatory synaptic strength. Currently we are actively pursuing this project. In addition, we have characterized a knockout mouse model developed by our collaborator at NIH, Dr. Katherine Roche.

Project Start
Project End
Budget Start
Budget End
Support Year
1
Fiscal Year
2012
Total Cost
$808,811
Indirect Cost
City
State
Country
Zip Code
Gu, Xinglong; Lu, Wei (2018) Genetic deletion of NMDA receptors suppresses GABAergic synaptic transmission in two distinct types of central neurons. Neurosci Lett 668:147-153
Yeh, Chia-Yu; Asrican, Brent; Moss, Jonathan et al. (2018) Mossy Cells Control Adult Neural Stem Cell Quiescence and Maintenance through a Dynamic Balance between Direct and Indirect Pathways. Neuron 99:493-510.e4
Steinkellner, Thomas; Zell, Vivien; Farino, Zachary J et al. (2018) Role for VGLUT2 in selective vulnerability of midbrain dopamine neurons. J Clin Invest 128:774-788
Li, Jun; Han, Wenyan; Pelkey, Kenneth A et al. (2017) Molecular Dissection of Neuroligin 2 and Slitrk3 Reveals an Essential Framework for GABAergic Synapse Development. Neuron 96:808-826.e8
Liu, Shuxi; Zhou, Liang; Yuan, Hongjie et al. (2017) A Rare Variant Identified Within the GluN2B C-Terminus in a Patient with Autism Affects NMDA Receptor Surface Expression and Spine Density. J Neurosci 37:4093-4102
Lu, Wei; Bromley-Coolidge, Samantha; Li, Jun (2017) Regulation of GABAergic synapse development by postsynaptic membrane proteins. Brain Res Bull 129:30-42
Mao, Xia; Gu, Xinglong; Lu, Wei (2017) GSG1L regulates the strength of AMPA receptor-mediated synaptic transmission but not AMPA receptor kinetics in hippocampal dentate granule neurons. J Neurophysiol 117:28-35
Han, Wenyan; Wang, Huiqing; Li, Jun et al. (2017) Ferric Chelate Reductase 1 Like Protein (FRRS1L) Associates with Dynein Vesicles and Regulates Glutamatergic Synaptic Transmission. Front Mol Neurosci 10:402
Lu, Wei; Chen, Yelin (2017) Development of fast neurotransmitter synapses: General principle and recent progress. Brain Res Bull 129:1-2
Gu, Xinglong; Zhou, Liang; Lu, Wei (2016) An NMDA Receptor-Dependent Mechanism Underlies Inhibitory Synapse Development. Cell Rep 14:471-478

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