C
Chiung Chun Huang
Researcher at National Cheng Kung University
Publications - 96
Citations - 4851
Chiung Chun Huang is an academic researcher from National Cheng Kung University. The author has contributed to research in topics: Long-term potentiation & Excitatory postsynaptic potential. The author has an hindex of 40, co-authored 96 publications receiving 4468 citations.
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Rap1-induced p38 Mitogen-activated Protein Kinase Activation Facilitates AMPA Receptor Trafficking via the GDI·Rab5 Complex POTENTIAL ROLE IN (S)-3,5-DIHYDROXYPHENYLGLYCINE-INDUCED LONG TERM DEPRESSION
TL;DR: An important role is suggested for Rap1-MKK3/6-p38 MAPK pathway in the induction of mGluR-dependent LTD by directly coupling to receptor trafficking machineries to facilitate the loss of synaptic AMPA receptors.
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Behavioral stress enhances hippocampal CA1 long-term depression through the blockade of the glutamate uptake.
TL;DR: It is found that selectively blocking NR2B-containing NMDA receptors (NMDARs) abolishes the induction of LTD by prolonged low-frequency stimulation (LFS) in slices from stressed animals, suggesting a novel role for glutamate-uptake machinery in the regulation of synaptic plasticity induction.
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Insulin Stimulates Postsynaptic Density-95 Protein Translation via the Phosphoinositide 3-Kinase-Akt-Mammalian Target of Rapamycin Signaling Pathway
TL;DR: In this article, the authors showed that insulin-induced increase in PSD-95 protein expression was inhibited by the tyrosine kinase inhibitor, AG1024, phosphatidylinositol 3-kinase (PI3K) inhibitors, LY294002 and wortmannin, translational inhibitors, anisomycin and rapamycin, but not by LY303511, and transcriptional inhibitor, actinomycin D.
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Insulin promotes dendritic spine and synapse formation by the PI3K/Akt/mTOR and Rac1 signaling pathways.
TL;DR: A novel role for IR signaling is revealed in the regulation of dendritic spine formation and excitatory synapse development in hippocampal neurons through activation of the PI3K/Akt/mTOR and Rac1 signaling pathways.
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Behavioral Stress Modifies Hippocampal Synaptic Plasticity through Corticosterone-Induced Sustained Extracellular Signal-Regulated Kinase/Mitogen-Activated Protein Kinase Activation
TL;DR: The results suggest that the effects of stress on LTP and LTD originate from the corticosterone-induced sustained activation of ERK1/2-coupled signaling cascades.