The lab is interested in understanding molecular and cellular mechanisms underlying synapse formation and synaptic plasticity, and in the long term elucidating synaptic mechanisms underlying neuronal circuit function in animal behavior. We believe that these studies 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 2013 fiscal year, we have added another dual whole cell patch-clamp system in the lab for electrophysiological analysis of neuronal activity. We have also established ultra fast drug application system in the lab to study ion channel kinetics and optimized in utero cDNA electroporation at E14 to manipulate neuronal gene expression. In addition, we established several rodent animal behavioral paradigms in the lab, which allow us to study hippocampus-dependent learning and memory. Installation of these equipment and methodologies in the lab allow us to efficiently pursue our scientific goals. On the research side, we have successfully determined the role of a novel protein in the regulation of excitatory synaptic strength with a combination of electrophysiological, molecular and cellular biological and genetic approaches. Currently we are studying biochemical mechanisms underlying its function. In addition, the second line of research in the lab has revealed some key molecular events underlying synapse formation. Currently we are actively pursuing this project to determine molecular pathways involved in this process. In addition, we are collaborating with Dr. Katherine Roches group at NINDS, NIH to study AMPA receptor trafficking. We are also collaborating with Dr. Francis McMahons group at NIMH, NIH to study neuronal activity in iPSC-derived neurons.
|Lussier, Marc P; Gu, Xinglong; Lu, Wei et al. (2014) Casein kinase 2 phosphorylates GluA1 and regulates its surface expression. Eur J Neurosci 39:1148-58|