• Complex
  • Title
  • Author
  • Keyword
  • Abstract
  • Scholars
High Impact Results & Cited Count Trend for Year Keyword Cloud and Partner Relationship

Query:

学者姓名:卓敏

Refining:

Indexed by

Submit Unfold

Co-Author

Submit Unfold

Language

Submit

Clean All

Export Sort by:
Default
  • Default
  • Title
  • Year
  • WOS Cited Count
  • Impact factor
  • Ascending
  • Descending
< Page ,Total 6 >
Rapid Turnover of Cortical NCAM1 Regulates Synaptic Reorganization after Peripheral Nerve Injury SCIE PubMed Scopus
期刊论文 | 2018 , 22 (3) , 748-759 | CELL REPORTS
WoS CC Cited Count: 2
Abstract&Keyword Cite

Abstract :

Peripheral nerve injury can induce pathological conditions that lead to persistent sensitized nociception. Although there is evidence that plastic changes in the cortex contribute to this process, the underlying molecular mechanisms are unclear. Here, we find that activation of the anterior cingulate cortex (ACC) induced by peripheral nerve injury increases the turnover of specific synaptic proteins in a persistent manner. We demonstrate that neural cell adhesion molecule 1 (NCAM1) is one of the molecules involved and show that it mediates spine reorganization and contributes to the behavioral sensitization. We show striking parallels in the underlying mechanism with the maintenance of NMDA-receptor- and protein-synthesis-dependent long-term potentiation (LTP) in the ACC. Our results, therefore, demonstrate a synaptic mechanism for cortical reorganization and suggest potential avenues for neuropathic pain treatment.

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Ko, Hyoung-Gon , Choi, Jun-Hyeok , Park, Dong Ik et al. Rapid Turnover of Cortical NCAM1 Regulates Synaptic Reorganization after Peripheral Nerve Injury [J]. | CELL REPORTS , 2018 , 22 (3) : 748-759 .
MLA Ko, Hyoung-Gon et al. "Rapid Turnover of Cortical NCAM1 Regulates Synaptic Reorganization after Peripheral Nerve Injury" . | CELL REPORTS 22 . 3 (2018) : 748-759 .
APA Ko, Hyoung-Gon , Choi, Jun-Hyeok , Park, Dong Ik , Kang, SukJae Joshua , Lim, Chae-Seok , Sim, Su-Eon et al. Rapid Turnover of Cortical NCAM1 Regulates Synaptic Reorganization after Peripheral Nerve Injury . | CELL REPORTS , 2018 , 22 (3) , 748-759 .
Export to NoteExpress RIS BibTex
Reduced synaptic function of Kainate receptors in the insular cortex of Fmr1 Knock-out mice SCIE PubMed Scopus
期刊论文 | 2018 , 11 | MOLECULAR BRAIN
Abstract&Keyword Cite

Abstract :

Fragile X syndrome is caused by the loss of fragile X mental retardation protein (FMRP). Kainate receptor (KAR) is a subfamily of ionotropic glutamate receptors (iGluR) that acts mainly as a neuromodulator of synaptic transmission and neuronal excitability. However, little is known about the changes of synaptic KAR in the cortical area of Fmr1 KO mice. In this study, we performed whole-cell patch-clamp recordings from layer II/III pyramidal neurons in the insular cortex of Fmr1 KO mice. We found that KARs mediated currents were reduced in Fmr1 KO mice. KARs were mainly located in the synaptosomal fraction of the insular cortex. The abundance of KAR subunit GluK1 and GluK2/3 in the synaptosome was reduced in Fmr1 KO mice, whereas the total expressions of these KARs subunits were not changed. Finally, lack of FMRP impairs subsequent internalization of surface GluK2 after KAR activation, while having no effect on the surface GluK2 expression. Our studies provide evidence indicating that loss of FMRP leads to the abnormal function and localization of KARs. This finding implies a new molecular mechanism for Fragile X syndrome.

Keyword :

Internalization Fragile X syndrome GluK2 Kainate receptor GluK1 Insular cortex FMRP

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Qiu, Shuang , Wu, Yu , Lv, Xinyou et al. Reduced synaptic function of Kainate receptors in the insular cortex of Fmr1 Knock-out mice [J]. | MOLECULAR BRAIN , 2018 , 11 .
MLA Qiu, Shuang et al. "Reduced synaptic function of Kainate receptors in the insular cortex of Fmr1 Knock-out mice" . | MOLECULAR BRAIN 11 (2018) .
APA Qiu, Shuang , Wu, Yu , Lv, Xinyou , Li, Xia , Zhuo, Min , Koga, Kohei . Reduced synaptic function of Kainate receptors in the insular cortex of Fmr1 Knock-out mice . | MOLECULAR BRAIN , 2018 , 11 .
Export to NoteExpress RIS BibTex
Neuronal and microglial mechanisms for neuropathic pain in the spinal dorsal horn and anterior cingulate cortex. PubMed Scopus
期刊论文 | 2017 , 141 (4) , 486-498 | Journal of neurochemistry | IF: 4.609
Abstract&Keyword Cite

Abstract :

Neuropathic pain is a debilitating chronic pain condition occurring after damage in the nervous system and is refractory to the currently available treatments. Major challenges include elucidating its mechanisms and developing new medications to treat it. Nerve injury-induced pain hypersensitivity involves aberrant excitability in spinal dorsal horn (SDH) neurons as a consequence of dysfunction of inhibitory interneurons and of hyperactivity of glial cells, especially microglia, the immune cells of the central nervous system. Evidence of this is found using animal models to investigate the molecular and cellular mechanisms of neuropathic pain. The pathologically altered somatosensory signals in the SDH then convey to the brain regions, including the anterior cingulate cortex (ACC). In these regions, nerve injury produces pre- and postsynaptic long-term plasticity, which contributes to negative emotions and anxiety associated with chronic pain conditions. Furthermore, recent evidence also indicates that the descending projection pathways from the ACC directly and indirectly to the SDH (the top-down corticospinal network) regulate nociceptive sensory transmission in the SDH. Thus, understanding a possible connection between the SDH and ACC, including a neuron-microglia interaction, may provide us with insights into the mechanisms used to amplify pain signals related to neuropathic pain and clues to aid the development of new therapeutic agents for the management of chronic pain. This article is part of the special article series "Pain".

Keyword :

spinal dorsal horn neurons top-down modulation synaptic plasticity microglia neuropathic pain anterior cingulate cortex

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Tsuda Makoto , Koga Kohei , Chen Tao et al. Neuronal and microglial mechanisms for neuropathic pain in the spinal dorsal horn and anterior cingulate cortex. [J]. | Journal of neurochemistry , 2017 , 141 (4) : 486-498 .
MLA Tsuda Makoto et al. "Neuronal and microglial mechanisms for neuropathic pain in the spinal dorsal horn and anterior cingulate cortex." . | Journal of neurochemistry 141 . 4 (2017) : 486-498 .
APA Tsuda Makoto , Koga Kohei , Chen Tao , Zhuo Min . Neuronal and microglial mechanisms for neuropathic pain in the spinal dorsal horn and anterior cingulate cortex. . | Journal of neurochemistry , 2017 , 141 (4) , 486-498 .
Export to NoteExpress RIS BibTex
Calcium-stimulated adenylyl cyclase subtype 1 (AC1) contributes to LTP in the insular cortex of adult mice. PubMed
期刊论文 | 2017 , 3 (7) , e00338 | Heliyon
Abstract&Keyword Cite

Abstract :

Long-term potentiation (LTP) of synaptic transmission in the central nervous system is a key form of cortical plasticity. The insular cortex (IC) is known to play important roles in pain perception, aversive memory and mood disorders. LTP has been recently reported in the IC, however, the signaling pathway for IC LTP remains unknown. Here, we investigated the synaptic mechanism of IC LTP. We found that IC LTP induced by the pairing protocol was N-methyl-D-aspartate receptors (NMDARs) dependent, and expressed postsynaptically, since paired-pulse ratio (PPR) was not affected. Postsynaptic calcium is important for the induction of post-LTP, since the postsynaptic application of BAPTA completely blocked the induction of LTP. Calcium-activated adenylyl cyclase subtype 1 (AC1) is required for potentiation. By contrast, AC8 is not required. Inhibition of Ca<sup>2+</sup> permeable α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (CP-AMPARs) or protein kinase M zeta (PKMζ) reduced the expression of LTP. Our results suggest that calcium-stimulated AC1, but not AC8, can be a trigger of the induction and maintenance of LTP in the IC.

Keyword :

Neuroscience

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Yamanaka Manabu , Matsuura Takanori , Pan Haili et al. Calcium-stimulated adenylyl cyclase subtype 1 (AC1) contributes to LTP in the insular cortex of adult mice. [J]. | Heliyon , 2017 , 3 (7) : e00338 .
MLA Yamanaka Manabu et al. "Calcium-stimulated adenylyl cyclase subtype 1 (AC1) contributes to LTP in the insular cortex of adult mice." . | Heliyon 3 . 7 (2017) : e00338 .
APA Yamanaka Manabu , Matsuura Takanori , Pan Haili , Zhuo Min . Calcium-stimulated adenylyl cyclase subtype 1 (AC1) contributes to LTP in the insular cortex of adult mice. . | Heliyon , 2017 , 3 (7) , e00338 .
Export to NoteExpress RIS BibTex
Ionotropic glutamate receptors contribute to pain transmission and chronic pain SCIE PubMed Scopus
期刊论文 | 2017 , 112 , 228-234 | NEUROPHARMACOLOGY | IF: 4.249
WoS CC Cited Count: 14
Abstract&Keyword Cite

Abstract :

Investigation of the synaptic mechanisms for sensory transmission and modulation provide us with critical information about the transmission of painful sensation as well as the basic mechanisms of chronic pain. Recent studies consistently demonstrate that glutamatergic synapses not only play an important role in sensory transmission, including pain and itch transmission, but also contribute to nociceptive sensitization at different levels of the brain. Different subtypes of glutamate receptors play selective roles in synaptic transmission and long-term potentiation (LTP), as well as synaptic modulation. Understanding the contribution of each subtype of glutamate receptors, and related downstream signaling pathways may provide a new opportunity to design better medicine for the treatment of different forms of chronic pain. This article is part of the Special Issue entitled 'Ionotropic glutamate receptors'. (C) 2016 Elsevier Ltd. All rights reserved.

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Zhuo, Min . Ionotropic glutamate receptors contribute to pain transmission and chronic pain [J]. | NEUROPHARMACOLOGY , 2017 , 112 : 228-234 .
MLA Zhuo, Min . "Ionotropic glutamate receptors contribute to pain transmission and chronic pain" . | NEUROPHARMACOLOGY 112 (2017) : 228-234 .
APA Zhuo, Min . Ionotropic glutamate receptors contribute to pain transmission and chronic pain . | NEUROPHARMACOLOGY , 2017 , 112 , 228-234 .
Export to NoteExpress RIS BibTex
Characterization of excitatory synaptic transmission in the anterior cingulate cortex of adult tree shrew SCIE PubMed Scopus
期刊论文 | 2017 , 10 | MOLECULAR BRAIN | IF: 3.449
Abstract&Keyword Cite

Abstract :

The tree shrew, as a primate-like animal model, has been used for studying high brain functions such as social emotion and spatial learning memory. However, little is known about the excitatory synaptic transmission in cortical brain areas of the tree shrew. In the present study, we have characterized the excitatory synaptic transmission and intrinsic properties of pyramidal neurons in the anterior cingulate cortex (ACC) of the adult tree shrew, a key cortical region for pain perception and emotion. We found that glutamate is the major excitatory transmitter for fast synaptic transmission. Excitatory synaptic responses induced by local stimulation were mediated by AMPA and kainate (KA) receptors. As compared with mice, AMPA and KA receptor mediated responses were significantly greater. Interestingly, the frequency of spontaneous excitatory postsynaptic currents (sEPSCs) and miniature excitatory postsynaptic currents (mEPSCs) in tree shrews was significantly less than that of mice. Moreover, both the ratio of paired-pulse facilitation (PPF) and the time of 50% decay for fast blockade of NMDA receptor mediated EPSCs were greater in the tree shrew. Finally, tree shrew neurons showed higher initial firing frequency and neuronal excitability with a cell type-specific manner in the ACC. Our studies provide the first report of the basal synaptic transmission in the ACC of adult tree shrew.

Keyword :

Calcium signals Intrinsic properties Tree shrew Excitatory synaptic transmission Anterior cingulate cortex Glutamate

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Li, Xu-Hui , Song, Qian , Chen, Qi-Yu et al. Characterization of excitatory synaptic transmission in the anterior cingulate cortex of adult tree shrew [J]. | MOLECULAR BRAIN , 2017 , 10 .
MLA Li, Xu-Hui et al. "Characterization of excitatory synaptic transmission in the anterior cingulate cortex of adult tree shrew" . | MOLECULAR BRAIN 10 (2017) .
APA Li, Xu-Hui , Song, Qian , Chen, Qi-Yu , Lu, Jing-Shan , Chen, Tao , Zhuo, Min . Characterization of excitatory synaptic transmission in the anterior cingulate cortex of adult tree shrew . | MOLECULAR BRAIN , 2017 , 10 .
Export to NoteExpress RIS BibTex
Characterization of serotonin-induced inhibition of excitatory synaptic transmission in the anterior cingulate cortex SCIE PubMed Scopus
期刊论文 | 2017 , 10 | MOLECULAR BRAIN | IF: 3.449
Abstract&Keyword Cite

Abstract :

Excitatory synaptic transmission in central synapses is modulated by serotonin (5-HT). The anterior cingulate cortex (ACC) is an important cortical region for pain perception and emotion. ACC neurons receive innervation of projecting serotonergic nerve terminals from raphe nuclei, but the possible effect of 5-HT on excitatory transmission in the ACC has not been investigated. In the present study, we investigated the role of 5-HT on glutamate neurotransmission in the ACC slices of adult mice. Bath application of 5-HT produced dose-dependent inhibition of evoked excitatory postsynaptic currents (eEPSCs). Paired pulse ratio (PPR) was significantly increased, indicating possible presynaptic effects of 5-HT. Consistently, bath application of 5-HT significantly decreased the frequency of spontaneous and miniature excitatory postsynaptic currents (sEPSCs and mEPSCs). By contrast, amplitudes of sEPSCs and mEPSCs were not significantly affected. After postsynaptic application of G protein inhibitor GDP-beta-S, 5-HT produced inhibition of eEPSCs was significantly reduced. Finally, NAN-190, an antagonist of 5-HT1A receptor, significantly reduced postsynaptic inhibition of 5-HT and abolished presynaptic inhibition. Our results strongly suggest that presynaptic as well as postsynaptic 5-HT receptor including 5-HT1A subtype receptor may contribute to inhibitory modulation of glutamate release as well as postsynaptic responses in the ACC.

Keyword :

Anterior cingulate cortex Serotonin Adenylyl cyclase Excitatory postsynaptic currents Glutamatergic neurotransmission

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Tian, Zhen , Yamanaka, Manabu , Bernabucci, Matteo et al. Characterization of serotonin-induced inhibition of excitatory synaptic transmission in the anterior cingulate cortex [J]. | MOLECULAR BRAIN , 2017 , 10 .
MLA Tian, Zhen et al. "Characterization of serotonin-induced inhibition of excitatory synaptic transmission in the anterior cingulate cortex" . | MOLECULAR BRAIN 10 (2017) .
APA Tian, Zhen , Yamanaka, Manabu , Bernabucci, Matteo , Zhao, Ming-gao , Zhuo, Min . Characterization of serotonin-induced inhibition of excitatory synaptic transmission in the anterior cingulate cortex . | MOLECULAR BRAIN , 2017 , 10 .
Export to NoteExpress RIS BibTex
Descending facilitation: From basic science to the treatment of chronic pain SCIE PubMed Scopus
期刊论文 | 2017 , 13 | MOLECULAR PAIN | IF: 3.205
WoS CC Cited Count: 5
Abstract&Keyword Cite

Abstract :

It is documented that sensory transmission, including pain, is subject to endogenous inhibitory and facilitatory modulation at the dorsal horn of the spinal cord. Descending facilitation has received a lot of attention, due to its potentially important roles in chronic pain. Recent investigation using neurobiological approaches has further revealed the link between cortical potentiation and descending facilitation. Cortical-spinal top-down facilitation, including those relayed through brainstem neurons, provides powerful control for pain transmission at the level of the spinal cord. It also provides the neuronal basis to link emotional disorders such as anxiety, depression, and loss of hope to somatosensory pain and sufferings. In this review, I will review a brief history of the discovery of brainstem-spinal descending facilitation and explore new information and hypothesis for descending facilitation in chronic pain.

Keyword :

Descending facilitation chronic pain pain serotonin anterior cingulate cortex mice rostroventral medial medulla

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Zhuo, Min . Descending facilitation: From basic science to the treatment of chronic pain [J]. | MOLECULAR PAIN , 2017 , 13 .
MLA Zhuo, Min . "Descending facilitation: From basic science to the treatment of chronic pain" . | MOLECULAR PAIN 13 (2017) .
APA Zhuo, Min . Descending facilitation: From basic science to the treatment of chronic pain . | MOLECULAR PAIN , 2017 , 13 .
Export to NoteExpress RIS BibTex
SCRAPPER Selectively Contributes to Spontaneous Release and Presynaptic Long-Term Potentiation in the Anterior Cingulate Cortex SCIE PubMed Scopus
期刊论文 | 2017 , 37 (14) , 3887-3895 | JOURNAL OF NEUROSCIENCE | IF: 5.97
WoS CC Cited Count: 5
Abstract&Keyword Cite

Abstract :

SCRAPPER is an E3 ubiquitin ligase expressed in presynaptic terminals, neural cell body, and dendrites of the hippocampus and cortex, which is coded by the FBXL20 gene. SCRAPPER is known to regulate synaptic transmissions and long-term potentiation (LTP) in the hippocampus, but no report is available for the cortex. Here we show genetic evidence for critical roles of SCRAPPER in excitatory transmission and presynaptic LTP (pre-LTP) of the anterior cingulate cortex (ACC), a critical cortical region for pain, anxiety, and fear. Miniature and spontaneous releases, but not evoked release, of glutamate were significantly increased in SCRAPPER knock-out (SCR-KO) mice. Interestingly, SCRAPPER selectively contributes to the increases of frequency and amplitude. The pre-LTP in the ACC was completely blocked in SCR-KO mice. Our results thus provide direct evidence for SCRAPPER in both spontaneous release and pre-LTP in the ACC and reveal a potential novel target for treating anxiety-related disease.

Keyword :

LTP presynaptic scrapper spontaneous release knock-out mice cortex

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Koga, Kohei , Yao, Ikuko , Setou, Mitsutoshi et al. SCRAPPER Selectively Contributes to Spontaneous Release and Presynaptic Long-Term Potentiation in the Anterior Cingulate Cortex [J]. | JOURNAL OF NEUROSCIENCE , 2017 , 37 (14) : 3887-3895 .
MLA Koga, Kohei et al. "SCRAPPER Selectively Contributes to Spontaneous Release and Presynaptic Long-Term Potentiation in the Anterior Cingulate Cortex" . | JOURNAL OF NEUROSCIENCE 37 . 14 (2017) : 3887-3895 .
APA Koga, Kohei , Yao, Ikuko , Setou, Mitsutoshi , Zhuo, Min . SCRAPPER Selectively Contributes to Spontaneous Release and Presynaptic Long-Term Potentiation in the Anterior Cingulate Cortex . | JOURNAL OF NEUROSCIENCE , 2017 , 37 (14) , 3887-3895 .
Export to NoteExpress RIS BibTex
Cortical kainate receptors and behavioral anxiety SCIE PubMed Scopus
期刊论文 | 2017 , 10 | MOLECULAR BRAIN | IF: 3.449
WoS CC Cited Count: 3
Abstract&Keyword Cite

Abstract :

The study of glutamatergic synapses mainly focuses on the memory-related hippocampus. Recent studies in the cortical areas such as the anterior cingulate cortex (ACC) show that excitatory synapses can undergo long-term plastic changes in adult animals. Long-term potentiation (LTP) of cortical synapses may play important roles in chronic pain and anxiety. In addition to NMDA and AMPA receptors, kainate (KA) receptors have been found to play roles in synaptic transmission, regulation and presynaptic forms of LTP. In this brief review, I will summarize the new progress made on KA receptors, and propose that ACC synapses may provide a good synaptic model for understanding cortical mechanism for behavioral anxiety, and its related emotional disorders.

Cite:

Copy from the list or Export to your reference management。

GB/T 7714 Zhuo, Min . Cortical kainate receptors and behavioral anxiety [J]. | MOLECULAR BRAIN , 2017 , 10 .
MLA Zhuo, Min . "Cortical kainate receptors and behavioral anxiety" . | MOLECULAR BRAIN 10 (2017) .
APA Zhuo, Min . Cortical kainate receptors and behavioral anxiety . | MOLECULAR BRAIN , 2017 , 10 .
Export to NoteExpress RIS BibTex
10| 20| 50 per page
< Page ,Total 6 >

Export

Results:

Selected

to

Format:
FAQ| About| Online/Total:3223/48836980
Address:XI'AN JIAOTONG UNIVERSITY LIBRARY(No.28, Xianning West Road, Xi'an, Shaanxi Post Code:710049) Contact Us:029-82667865
Copyright:XI'AN JIAOTONG UNIVERSITY LIBRARY Technical Support:Beijing Aegean Software Co., Ltd.