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 brains and psychiatric disorders. Dr. Li’s group employs a combination of optical imaging (two-photon and confocal), in vivo and ex vivo electrophysiology, behavioral, optogenetic, and molecular biological approaches to identify molecules and signaling pathways that control the function, structure, and plasticity of synapses. Dr. Li’s group at the NIMH has discovered: (1) a novel mitochondria, caspase, and autophagy-mediated pathway for long-term depression of synaptic transmission, control of synaptic vesicle pools, and the consolidation of contextual fear memory; (2) a new age-dependent function of dopamine D2 receptors in the development of dendritic spines and working memory; (3) a new role of mitochondrial fission in gamma oscillations; (4) mitophagy as an essential cellular process underlying psychogenic stress-induced synaptic weakening in the anxiolytic circuit; (5) miRNAs involved in long-lasting synaptic plasticity. These findings shed new light on the fundamental questions of how intracellular signaling cascades control the establishment of synaptic connections, modification of synaptic strength, and response to psychogenic stress. Dr. Li’s current research focuses on mitochondria-mediated mechanisms in supporting and modulating synaptic plasticity and synaptic activities. See Dr. Li’s publications on her NIH National Center for Biotechnology Information (NCBI) bibliography page.
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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