Zhao DQ, Xue H, Sun HJ. Nervous mechanisms of restraint water-immersion stress-induced gastric mucosal lesion. World J Gastroenterol 2020; 26(20): 2533-2549 [PMID: 32523309 DOI: 10.3748/wjg.v26.i20.2533]
Corresponding Author of This Article
Hai-Ji Sun, PhD, Associate Professor, Key Laboratory of Animal Resistance of Shandong Province, College of Life Sciences, Shandong Normal University, No. 88, East Wenhua Road, Lixia District, Jinan 250014, Shandong Province, China. 109127@sdnu.edu.cn
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. May 28, 2020; 26(20): 2533-2549 Published online May 28, 2020. doi: 10.3748/wjg.v26.i20.2533
Nervous mechanisms of restraint water-immersion stress-induced gastric mucosal lesion
Dong-Qin Zhao, Hua Xue, Hai-Ji Sun
Dong-Qin Zhao, Hua Xue, Hai-Ji Sun, Key Laboratory of Animal Resistance of Shandong Province, College of Life Sciences, Shandong Normal University, Jinan 250014, Shandong Province, China
Author contributions: Xue H was responsible for the collection of references; Sun HJ wrote the part of peripheral nervous mechanism of RWIS-induced GML experiments; Zhao DQ wrote the central mechanism of RWIS-induced GML and was responsible for the entire manuscript; all the authors approved the final version of the manuscript for publication.
Supported byNational Natural Science Foundation of China, No. 31501861 and No. 31672286; and Natural Science Foundation of Shandong Province, China, No. ZR2015CM013.
Conflict-of-interest statement: The authors declare no conflicts of interest.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Hai-Ji Sun, PhD, Associate Professor, Key Laboratory of Animal Resistance of Shandong Province, College of Life Sciences, Shandong Normal University, No. 88, East Wenhua Road, Lixia District, Jinan 250014, Shandong Province, China. 109127@sdnu.edu.cn
Received: December 23, 2019 Peer-review started: December 23, 2019 First decision: April 1, 2020 Revised: April 7, 2020 Accepted: April 29, 2020 Article in press: April 29, 2020 Published online: May 28, 2020 Processing time: 157 Days and 10.5 Hours
Core Tip
Core tip: The nervous mechanisms of gastric mucosal lesion in rats subjected to restraint water-immersion stress were investigated. Abnormal regulation of the enteric nervous system, mainly due to the enhanced activity of the parasympathetic nervous system, can induce gastrointestinal dysfunction. The central nucleus such as dorsal motor nucleus of the vagus, nucleus ambiguous, nucleus of the solitary tract, paraventricular nucleus, supraoptic nucleus, mediodorsal nucleus of the thalamus, central nucleus of the amygdala and medial prefrontal cortex are all involved in the formation of stress-induced gastric mucosal lesion. Nitric oxide, 5-hydroxytryptamine, hydrogen sulfide, calcitonin gene-related peptide, vasoactive intestinal peptide, acetylcholine, catecholamine, glutamate, γ-aminobutyric acid, oxytocin and arginine vasopressin may be involved in the physiological process.
