Zheng Li, Ph.D.
Section on Synapse Development Plasticity
Dr. Zheng Li received a Ph.D. degree from the State University of New York at Stony Brook. Her graduate studies on the role of Rho GTPases in dendrite morphogenesis were carried out with Hollis Cline at Cold Spring Harbor Laboratory. She obtained postdoctoral training on synapse development and plasticity with Morgan Sheng at Massachusetts Institute of Technology. Dr. Li joined NIMH as an Investigator in 2006.
The research interest of Dr. Zheng Li is the molecular and cellular mechanisms of synapse development and plasticity in normal and schizophrenic brains. Dr. Zheng Li’s group employs a combination of optical imaging (two-photon and confocal), electrophysiology, behavioral and genomic approaches to identify molecules and signaling pathways that control the function, structure and plasticity of synapses. Currently Dr. Zheng Li’s research is focusing on two areas: (1) the induction of mechanism of long-term depression of synaptic transmission (LTD, a form of synaptic plasticity that leads to the weakening of synaptic response and synapse loss and is important for brain development and cognition); and (2) the function of schizophrenia risk genes in regulating synapse development and plasticity. Dr. Zheng Li’s group mainly conducts experiments with hippocampal neurons. The hippocampus is a brain structure essential for cognitive functions (e.g. learning and memory) and has been implicated in the pathophysiology of schizophrenia. Dr. Zheng Li’s group has recently uncovered a novel mechanism for LTD induction in hippocampal neurons which is mediated by caspases. Caspases have well-known functions in apoptosis. However, the findings from Dr. Zheng Li’s lab suggest that in normal hippocampal neuron caspases activate the key cellular process that is responsible for reducing synaptic strength without causing cell death. In addition to normal synaptic plasticity, the work from Dr. Zheng Li’s group indicates that some schizophrenia risk genes are important regulators of the structural and functional maturation of synapses, which provides insights to the neuronal basis of reduced mental performance associated with schizophrenia.
Jiao S, Li Z (2011). Nonapoptotic function of BAD and BAX in long-term depression of synaptic transmission. Neuron 70, 758-72. https://doi.org/10.1016/j.neuron.2011.04.004. [Pubmed Link]
Jia JM, Zhao J, Hu Z, Lindberg D, Li Z (2013). Age-dependent regulation of synaptic connections by dopamine D2 receptors. Nat Neurosci 16, 1627-36. https://doi.org/10.1038/nn.3542. [Pubmed Link]
Hu Z, Yu D, Gu QH, Yang Y, Tu K, Zhu J, Li Z (2014). miR-191 and miR-135 are required for long-lasting spine remodelling associated with synaptic long-term depression. Nat Commun 5, 3263. https://doi.org/10.1038/ncomms4263. [Pubmed Link]
Shen H, Zhu H, Panja D, Gu Q, Li Z (2020). Autophagy controls the induction and developmental decline of NMDAR-LTD through endocytic recycling. Nat Commun 11, 2979. https://doi.org/10.1038/s41467-020-16794-5. [Pubmed Link]
Nordman JC, Ma X, Gu Q, Potegal M, Li H, Kravitz AV, Li Z (2020). Potentiation of Divergent Medial Amygdala Pathways Drives Experience-Dependent Aggression Escalation. J Neurosci 40, 4858-4880. https://doi.org/10.1523/JNEUROSCI.0370-20.2020. [Pubmed Link]
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