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Your search keyword '"Zeng, Menglong"' showing total 22 results
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22 results on '"Zeng, Menglong"'

1. Long-term potentiation reconstituted with an artificial TARP/PSD-95 complex

Author

Ravi, Anagh Sinha, Zeng, Menglong, Chen, Xudong, Sandoval, Gerardo, Diaz-Alonso, Javier, Zhang, Mingjie, and Nicoll, Roger A

Subjects
Biochemistry and Cell Biology, Biological Sciences, Neurosciences, Genetics, 1.1 Normal biological development and functioning, Underpinning research, Disks Large Homolog 4 Protein, Long-Term Potentiation, Nuclear Proteins, Receptors, AMPA, Synapses, Synaptic Transmission, AMPA receptor trafficking, AMPAR, CP: Neuroscience, GluA1, LTP, MAGUK, PSD-95, TARP, postsynaptic density, synaptic transmission, Medical Physiology, Biological sciences
Abstract

The critical role of AMPA receptor (AMPAR) trafficking in long-term potentiation (LTP) of excitatory synaptic transmission is now well established, but the underlying molecular mechanism is still uncertain. Recent research suggests that PSD-95 captures AMPARs via an interaction with the AMPAR auxiliary subunits-transmembrane AMPAR regulatory proteins (TARPs). To determine if such interaction is a core minimal component of the AMPAR trafficking and LTP mechanism, we engineered artificial binding partners, which individually were biochemically and functionally dead but which, when expressed together, rescue binding and both basal synaptic transmission and LTP. These findings establish the TARP/PSD-95 complex as an essential interaction underlying AMPAR trafficking and LTP.

Published
2022

16. Anchoring high concentrations of SynGAP at postsynaptic densities via liquid-liquid phase separation.

Author

Zeng, Menglong, Bai, Guanhua, and Zhang, Mingjie

Subjects
*DENDRITIC spines, *PHASE separation, *POSTSYNAPTIC density protein, *NERVOUS system, *GUANOSINE triphosphatase, *INTELLECTUAL disabilities
Abstract

SynGAP, encoded by SYNGAP1, is a Ras/Rap GTPase activator specifically expressed in the nervous systems. SynGAP is one of the most abundant proteins in the postsynaptic densities (PSDs) of excitatory synapses and acts as a critical synaptic activity brake by tuning down synaptic GTPase activities. Mutations of SYNGAP1 have been frequently linked to brain disorders including intellectual disability, autisms, and seizure. SynGAP has been shown to undergo fast dispersions from synapses in response to stimulations, a strategy that neurons use to control the specific activities of the enzyme within the tiny, semi-open compartments in dendritic spines. However, the mechanism governing the activity-dependent synaptic localization modulations of SynGAP is poorly understood. It has been shown recently that SynGAP α1, via specifically binding to PSD-95, can undergo liquid-liquid phase separation forming membraneless, condensed protein-rich sub-compartments. This phase transition-mediated, PSD-95-dependent synaptic enrichment of SynGAP α1 not only suggests a dynamic anchoring mechanism of the protein within the PSD, but also implies a new model for the PSD formation in living neurons. [ABSTRACT FROM AUTHOR]

Published
2019
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18. Mice with Shank3 Mutations Associated with ASD and Schizophrenia Display Both Shared and Distinct Defects

Author

Zhou, Yang, primary, Kaiser, Tobias, additional, Monteiro, Patrícia, additional, Zhang, Xiangyu, additional, Van der Goes, Marie. S., additional, Wang, Dongqing, additional, Barak, Boaz, additional, Zeng, Menglong, additional, Li, Chenchen, additional, Lu, Congyi, additional, Wells, Michael, additional, Amaya, Aldo, additional, Nguyen, Shannon, additional, Lewis, Michael, additional, Sanjana, Neville, additional, Zhou, Yongdi, additional, Zhang, Mingjie, additional, Zhang, Feng, additional, Fu, Zhanyan, additional, and Feng, Guoping, additional

Published
2016
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22. Mice with Shank3 Mutations Associated with ASD and Schizophrenia Display Both Shared and Distinct Defects

Author

Tobias Kaiser, Dongqing Wang, Michael F. Wells, Yang Zhou, Neville E. Sanjana, Aldo Amaya, Congyi Lu, Yongdi Zhou, Shannon Nguyen, Michael C. Lewis, Xiangyu Zhang, Mingjie Zhang, Marie Sophie van der Goes, Menglong Zeng, Zhanyan Fu, Guoping Feng, Boaz Barak, Chenchen Li, Patricia Monteiro, Feng Zhang, Massachusetts Institute of Technology. Department of Biological Engineering, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, McGovern Institute for Brain Research at MIT, Zhou, Yang, Kaiser, Tobias, Monteiro, Patricia, Zhang, Xiangyu, Van der Goes, Marie-Sophie, Wang, Dongqing, Barak, Boaz, Zeng, Menglong, Li, Chenchen, Lu, Congyi, Wells, Michael, Sanjana, Neville E, Zhang, Feng, Fu, Zhanyan, and Feng, Guoping

Subjects
0301 basic medicine, Genetics, Brain Diseases, Neuroscience(all), General Neuroscience, Transgene, Mutant, Neurotransmission, Biology, Phenotype, Article, 3. Good health, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Humans, Mass Media, Allele, Prefrontal cortex, Gene, Neuroscience, 030217 neurology & neurosurgery, Dominance (genetics)
Abstract

Genetic studies have revealed significant overlaps of risk genes among psychiatric disorders. However, it is not clear how different mutations of the same gene contribute to different disorders. We characterized two lines of mutant mice with Shank3 mutations linked to ASD and schizophrenia. We found both shared and distinct synaptic and behavioral phenotypes. Mice with the ASD-linked InsG3680 mutatio n manifest striatal synaptic transmission defects before weaning age and impaired juvenile social interaction, coinciding with the early onset of ASD symptoms. On the other hand, adult mice carrying the schizophrenia-linked R1117X mutation show profound synaptic defects in prefrontal cortex and social dominance behavior. Furthermore, we found differential Shank3 mRNA stability and SHANK1/2 upregulation in these two lines. These data demonstrate that different alleles of the same gene may have distinct phenotypes at molecular, synaptic, and circuit levels in mice, which may inform exploration of these relationships in human patients., National Institute of Mental Health (U.S.) (Grant 5R01MH097104), National Institute of Mental Health (U.S.) (Grant 5DP1-MH100706), National Institutes of Health (U.S.) (Grant R01-NS 07312401)

Published
2015

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