Activation of spinal Extacellular Signal‐Regulated Kinases and c‐jun N‐terminal kinase signaling pathways contributes to morphine‐induced acute and chronic hyperalgesia in mice-Reference-Cited by-同舟云学术

Activation of spinal Extacellular Signal‐Regulated Kinases and c‐jun N‐terminal kinase signaling pathways contributes to morphine‐induced acute and chronic hyperalgesia in mice

Published:2019-04-23 Issue:9 Volume:120 Page:15045-15056
ISSN:0730-2312
Container-title:Journal of Cellular Biochemistry
language:en
Short-container-title:J Cell Biochem

Author:

Ruan Jia‐Ping¹²,Chen Ling³^ORCID,Ma Zheng‐liang¹

Affiliation:

1. Department of Anesthesiology Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University Nanjing Jiangsu China

2. Affiliated Hospital of Integrated Traditional Chinese and Western Medicine Nanjing University of Chinese Medicine Nanjing Jiangsu China

3. Laboratory of Reproductive Medicine Nanjing Medical University Nanjing Jiangsu China

Publisher

Wiley

Subject

Cell Biology,Molecular Biology,Biochemistry

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/jcb.28766

Reference37 articles.

1. Opioid-Induced Hyperalgesia and Tolerance

2. An Emerging Role for the Delta Opioid Receptor in the Regulation of Mu Opioid Receptor Function

3. Acute thermal hyperalgesia elicited by low-dose morphine in normal mice is blocked by ultra-low-dose naltrexone, unmasking potent opioid analgesia

4. Low-dose morphine induces hyperalgesia through activation of Gαs, protein kinase C, and l-type Ca2+ channels in rats

5. Signaling pathway of morphine induced acute thermal hyperalgesia in mice

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