Jing Cao
Lanzhou University
5 Papers
42 Citations
Jing Cao is an academic researcher from Lanzhou University. The author has contributed to research in topics: NMDA receptor & Receptor. The author has an hindex of 3, co-authored 3 publications.
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Papers
NR2B phosphorylation at tyrosine 1472 in spinal dorsal horn contributed to N-methyl-D-aspartate-induced pain hypersensitivity in mice.
TL;DR: The data suggested that activation of spinal NMDARs was able to accumulate NR2BR at synapses via SFK signaling, which might exaggerate N MDAR‐dependent nociceptive transmission and contribute to NMDA‐induced nocICEptive behavioral hyperresponsiveness.
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GABAergic disinhibition induced pain hypersensitivity by upregulating NMDA receptor functions in spinal dorsal horn.
Jing Cao,Xian Yang,Yan-Ni Liu,Zhan-Wei Suo,Lei Shi,Cheng-Rong Zheng,Hongbin Yang,Shuai Li,Xiao-Dong Hu +8 more
TL;DR: Intathecal application of bicuculline to remove the inhibition of GABA(A) receptor antagonist readily elicited mechanical allodynia in naive mice, which could be dose-dependently attenuated by NMDARs antagonist D-APV, and suggested that removal of GABAergic inhibition allowed for PKA-mediated N MDARs phosphorylation and synaptic accumulation, thus exaggerating NMD ARs-dependent nociceptive transmission and behavioral sensitization.
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Cav3.2 T-Type calcium channels downregulation attenuates bone cancer pain induced by inhibiting IGF-1/HIF-1α signaling pathway in the rat spinal cord
Qingying Liu,Zhongyuan Lu,H. Ren,Lijun Fu,Yueliang Wang,Hui-Lian Bu,Minyu Ma,Letian Ma,Chen Huang,Jian Wang,Weidong Zang,Jing Cao,Xiaochong Fan +12 more
TL;DR: The role of Cav3.2 T-type calcium channel in alleviating pain hypersensitivity is achieved by inhibiting the IGF-1/HIF-1α signaling pathway and a positive regulation of Cav 3.2 by HIF- 1α at the transcriptional level is proposed.
2
cAMP-dependent protein kinase activated Fyn in spinal dorsal horn to regulate NMDA receptor function during inflammatory pain.
Hongbin Yang,Xian Yang,Jing Cao,Shuai Li,Yan-Ni Liu,Zhan-Wei Suo,Hong-Bin Cui,Zhong Guo,Zhong Guo,Xiao-Dong Hu +9 more
TL;DR: In this article, the authors showed that cAMP-dependent protein kinase (PKA) played an important role in redistributing GluN2BR at synapses, because inhibition of PKA activity impaired the accumulation at post-synaptic density (PSD)-enriched fraction in CFA-injected mice.
Inhibition of glutamatergic neurons in layer II/III of the medial prefrontal cortex alleviates paclitaxel-induced neuropathic pain and anxiety.
TL;DR: In this paper , the role of glutamatergic neurons in layer II/III of the medial prefrontal cortex (mPFC) in paclitaxel (4 mg/kg/d, consecutive 8 days, intraperitoneal injection, cumulative dose: 32 mg/ kg)induced pain and anxiety by using a combination of behavior testing's, immunostaining, chemogenetics, optogenetics and fiberphotometry, and morphological approaches.