Hongbing Wang, Ph.D.
My lab investigates the cellular and molecular mechanisms underlying synaptic modification and specific aspects of adaptive behavior. I hope that some outcomes from these basic and preclinical research directions may lead to therapeutic strategies for the treatment of pathological conditions, including intellectual disability, autism, and mood disorders.
The main research objectives are 1) identify molecular/cellular substrates and determinants in learning, re-learning, and forgetting; 2) identify molecular/cellular pathology and therapeutic approaches to treat Fragile X syndrome; 3) identify molecular pathways to control adaptive behaviors associated with mood disorders; 4) identify mechanisms to control transcription homeostasis in neurons.
The main approaches are 1) gene knockout and overexpression with transgenic mice; 2) transcription profiling with RNAseq and RT-PCR; 3) behavior analysis; 4) electrophysiology with ex vivo brain slices and in vivo with anesthetized mice; 5) optogenetics method to activate signaling molecules; 6) cellular model with primary neurons and glial cells; 7) cellular and tissue analysis with immunostaining and Western blot.
Miyoung Yang*, Qi Ding*, Ming Zhang, Changjong Moon, Hongbing Wang (2020) Forebrain overexpression of type 1 adenylyl cyclase promotes molecular stability and behavioral resilience to physical stress. Neurobiology of Stress. https://doi.org/10.1016/j.ynstr.2020.100237. * equal contribution.
Qi Ding, Ferzin Sethna, Xue-Ting Wu, Zhuang Miao, Ping Chen, Yueqi Zhang, Hua Xiao, Wei Feng, Yue Feng, Xuan Li, Hongbing Wang (2020) Transcriptome signature analysis repurposes trifluoperazine for the treatment of fragile X syndrome in mouse model. Communications Biology. Mar 16;3(1):127. doi: 10.1038/s42003-020-0833-4.
Ferzin Sethna, Wei Feng, Qi Ding, Alfred J. Robison, Yue Feng, Hongbing Wang (2017) Enhanced expression of ADCY1 underlies aberrant neuronal signaling and behavior in a syndromic autism model. Nature Communications. Feb 20;8:14359. doi: 10.1038/ncomms14359.
Fei Zheng, Ming Zhang, Qi Ding, Ferzin Sethna, Lily Yan, Changjong Moon, Miyoung Yang, and Hongbing Wang (2016) Voluntary running depreciates the requirement of Ca2+-stimulated cAMP signaling in synaptic potentiation and memory formation. Learn Mem. 23(8):442-9.
Xianju Zhou, Zhuoyou Chen, Wenwei Yun, J Ren, Chenwei Li, and Hongbing Wang (2015) Extrasynaptic NMDA Receptor in Excitotoxicity: Function Revisited. The Neuroscientist. (4):337-44.
Xianju Zhou1, Qi Ding, Zhuoyou Chen, Huifang Yun, and Hongbing Wang (2013) Involvement of GluN2A and GluN2B in synaptic and extrasynaptic NMDA receptor function and neuronal excitotoxicity. J Biol Chem. 288(33):24151-9.
Xianju Zhou, Daniel Hollern, Jiayu Liao, Eran Andrechek, and Hongbing Wang (2013) NMDA receptor-mediated excitotoxicity depends on the co-activation of synaptic and extrasynaptic receptors. Cell Death & Disease. 4:e560. doi: 10.1038/cddis.2013.82.
Ming Zhang and Hongbing Wang (2013) Mice overexpressing type 1 adenylyl cyclase show enhanced spatial memory flexibility in the absence of intact synaptic long-term depression. Learn Mem. 20: 352-357.
Ming Zhang, Daniel Storm, and Hongbing Wang. (2011) Bidirectional synaptic plasticity and spatial memory flexibility require Ca2+-stimulated adenylyl cyclases. J. Neurosci. 31(28): 10174-183.
Ming Zhang, Changjong Moon, Guy Chan, Lan Yang, Fei Zheng, Alana Conti, Lisa Muglia, Louis Muglia, Daniel Storm, and Hongbing Wang. (2008) Ca-stimulated type 8 adenylyl cyclase is required for rapid acquisition of novel spatial information and for working/episodic-like memory. J. Neurosci. 28 (18): 4736-4744.