L
Long Jun Wu
Researcher at Mayo Clinic
Publications - 159
Citations - 11833
Long Jun Wu is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Microglia & Long-term potentiation. The author has an hindex of 54, co-authored 157 publications receiving 9290 citations. Previous affiliations of Long Jun Wu include Harvard University & University of Toronto.
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Journal ArticleDOI
International Union of Basic and Clinical Pharmacology. LXXVI. Current Progress in the Mammalian TRP Ion Channel Family
TL;DR: Recent progress on the physiology, pharmacology and pathophysiological function of mammalian TRP channels is reviewed to indicate that these channels have broad function in physiology.
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Roles of NMDA NR2B Subtype Receptor in Prefrontal Long-Term Potentiation and Contextual Fear Memory
Ming Gao Zhao,Hiroki Toyoda,Yong-Seok Lee,Yong-Seok Lee,Long Jun Wu,Long Jun Wu,Shanelle W. Ko,Xue Han Zhang,Yongheng Jia,Fanny W.F. Shum,Hui Xu,Bao Ming Li,Bong-Kiun Kaang,Bong-Kiun Kaang,Min Zhuo,Min Zhuo +15 more
TL;DR: It is reported that the activation of the NR2B and NR2A subunits of the NMDA receptor is critical for the induction of cingulate LTP, regardless of the induction protocol.
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Neuronal Hyperactivity Recruits Microglial Processes via Neuronal NMDA Receptors and Microglial P2Y12 Receptors after Status Epilepticus
TL;DR: The results elucidate the molecular mechanisms underlying microglia–neuron communication that may be potentially neuroprotective in the epileptic brain and found that P2Y12 KO mice exhibited reduced seizure-induced increases in microglial process numbers and worsened KA-induced seizure behaviors.
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Presynaptic and Postsynaptic Amplifications of Neuropathic Pain in the Anterior Cingulate Cortex
Hui Xu,Long Jun Wu,Hansen Wang,Xuehan Zhang,Kunjumon I. Vadakkan,Susan S. Kim,Hendrik W. Steenland,Min Zhuo +7 more
TL;DR: It is reported that peripheral nerve injury triggered long-term changes in excitatory synaptic transmission in layer II/III neurons within the anterior cingulate cortex (ACC) and that AC1 is critical for such long- term changes.
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Deficits in Trace Fear Memory and Long-Term Potentiation in a Mouse Model for Fragile X Syndrome
TL;DR: It is demonstrated that FMR1 knock-out mice show a defect in trace fear memory without changes in locomotion, anxiety, and pain sensitivity, which suggests that synaptic plasticity in the ACC and amygdala of F MR1 KO mice plays an important role in the expression of behavioral phenotypes similar to the symptoms of fragile X syndrome.