Bo Li

Bo Li

 

Assistant Professor
Cold Spring Harbor Laboratory

PhD, The University of British Columbia

Phone: (516) 367-8485
bli@cshl.edu

 

 


Research

Dysfunction of glutamatergic synapses is believed to play an important role in the pathogenesis of major psychiatric disorders, including schizophrenia and depression. However, many key questions remain unclear such as: What are the causes of the glutamatergic synapse dysfunction? Where in the brain does this dysfunction occur? How does this result in the behavioral phenotypes? Recent advances in several areas have made it possible to directly address these questions. These include the identification of disease-linked genetic variants, the development of novel techniques to study a specific brain circuit, and the demonstration of the role of synaptic plasticity in adaptive behaviors. We are interested in studying normal synaptic plasticity and disease-related synaptic changes in the brain circuits involved in schizophrenia and depression, with the long-term goal of developing methods that will allow the manipulation of activity in specific brain circuits in order to change disease-related behaviors.

A number of complementing methodologies are being employed including patch-clamp recording and calcium imaging of labeled neurons, two-photon imaging of spine morphology and tagged receptors, in vivo virus injection, RNA interference (RNAi)-based gene silencing, activation of specific axon terminals using light-gated cation channels (ChR2), activation or silencing of specific brain regions using transgenes driven by regional specific promoters, as well as assessment of the behavioral consequences of certain manipulations. We hope these studies will shed light on the mechanisms that link the genetic deficits, synaptic dysfunction, and pathophysiology of major psychiatric disorders.

  • Publications
  • Laboratory Personnel
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    • Li, B.*, Devidze, N.,* Barengolts, D., Prostak, N., Sphicas, E., Apicella, A.J., Malinow, R., and Emamian, E.S. 2009. NMDA receptor phosphorylation at a site affected in schizophrenia controls synaptic and behavioral plasticity. The Journal of Neuroscience 29: 11965-11972.
    • Li, B., Woo, R.S., Mei, L., Malinow, R. 2007. The neuregulin1 receptor erbB4 controls glutamatergic synapse maturation and plasticity. Neuron 54: 583-597.
    • Kopec, C.D.,* Li, B.,* Wei, W., Boehm, J., Malinow, R. 2006. Glutamate receptor exocytosis and spine enlargement during chemically induced long-term potentiation. The Journal of Neuroscience 26: 2000-2009.
    • Li, B., Otsu, Y., Murphy, T.H. and Raymond, L.A. 2003. Developmental decrease in NMDA receptor desensitization associated with shift to synapse and interaction with PSD-95. The Journal of Neuroscience 23: 11244-11254.
    • Li, B., Chen, N., Luo, T., Otsu, Y., Murphy, T.H. and Raymond, L.A. 2002. Differential regulation of synaptic and extrasynaptic NMDA receptors. Nature Neuroscience 5: 833-834.
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