Basic Study
Copyright ©The Author(s) 2019. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. May 21, 2019; 25(19): 2315-2326
Published online May 21, 2019. doi: 10.3748/wjg.v25.i19.2315
Electroacupuncture at ST36 modulates gastric motility via vagovagal and sympathetic reflexes in rats
Meng-Jiang Lu, Zhi Yu, Yan He, Yin Yin, Bin Xu
Meng-Jiang Lu, Zhi Yu, Yan He, Yin Yin, Bin Xu, Key Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing 210023, Jiangsu Province, China
Author contributions: Yu Z and Lu MJ contributed equally to this work; Yu Z and Xu B conceived and designed the experiments; Lu MJ performed the experiments and wrote the paper; Yan H and Yin Y performed the experiments; Lu MJ and Yu Z analyzed the data; all authors read and approved the final version of the article to be published.
Supported by the National Natural Science Foundation of China, No. 81373749; No. 81574071, and No. 81673883.
Institutional review board statement: The study was reviewed and approved by the Institutional Review Board of the Nanjing University of Chinese Medicine.
Institutional animal care and use committee statement: All experimental manipulations were undertaken in accordance with the Guide for the Care and Use of Laboratory Animals (National Institutes of Health), and the study was approved by the Institutional Animal Care and Use Committee of Nanjing University of Chinese Medicine (No. 201805A017).
Conflict-of-interest statement: The authors declare that there are no conflicts of interest to disclose.
Data sharing statement: No additional unpublished data are available.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Open-Access: 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/
Corresponding author: Bin Xu, PhD, Professor, Key Laboratory of Integrated Acupuncture and Drugs, Nanjing University of Chinese Medicine, No. 138, Xianlin Road, Nanjing 210023, Jiangsu Province, China. xubin@njucm.edu.cn
Telephone: +86-132-5529-1963
Received: February 28, 2019
Peer-review started: March 1, 2019
First decision: April 4, 2019
Revised: April 22, 2019
Accepted: May 3, 2019
Article in press: May 3, 2019
Published online: May 21, 2019
ARTICLE HIGHLIGHTS
Research background

Electroacupuncture (EA) at ST36 can significantly improve gastrointestinal symptoms, especially in promoting gastrointestinal motility. The automatic nervous system plays a main role in EA at ST36, but few studies exist on how vagovagal and sympathetic reflexes affect EA in regulating gastrointestinal motility.

Research motivation

This study aimed to investigate the mechanism of the automatic nervous system in promoting gastrointestinal motility by EA at ST36. The results obtained may be used to explain the mechanism of EA in regulating gastrointestinal motility. Furthermore, it may provide a reference to neurostimulation therapy.

Research objectives

The objective of this study was to determine the role of vagovagal and sympathetic reflexes in EA at ST36, as well as the associated receptor subtypes that are involved. The results obtained may be used to explain the mechanism of EA in regulating gastrointestinal motility. Furthermore, it may provide a reference to neurostimulation therapy.

Research methods

Gastric motility was measured with a manometric balloon in anesthetized animals. The peripheral nervous activity was measured with a platinum electrode hooking the vagus or greater splanchnic nerve, and the central nervous activity was measured with a glass microelectrode in the DMV. The effects and mechanisms of EA at ST36 were explored in male Sprague-Dawley rats which were divided into a control group, vagotomy group, sympathectomy group, and microinjection group [including an artificial cerebrospinal fluid group, glutamate (L-Glu) group, and γ-aminobutyric acid (GABA) group] and in genetically modified male mice [β1β2 receptor-knockout (β1β2-/-) mice, M2M3 receptor-knockout (M2M3-/-) mice, and wild-type control mice].

Research results

EA at ST36 promoted gastric motility during 30-120 s. During EA, the vagus nerve activity was much higher than sympathetic activity. The gastric motility mediated by EA at ST36 was interdicted by vagotomy. However, the delay effect of EA during 0-30 s was eliminated by sympathectomy. EA at ST36 decreased gastric motility in M2/3-/- mice and promoted gastric motility in β1/2-/- mice. Extracellular recordings showed that EA at ST36 increased spikes of the dorsal motor nucleus of the vagus (DMV). Microinjection of L-Glu into the DMV increased gastric motility, while EA at ST36 decreased gastric motility during 0-60s, and promoted gastric motility during 60-120 s. Injection of GABA reduced or increased gastric motility, and reduced the gastric motility-promoting effect of EA at ST36.

Research conclusions

EA at ST36 modulates gastric motility via vagovagal and sympathetic reflexes mediated through M2/3 and β1/2 receptors, respectively. Sympathetic nerve activity mediated through β1/2 receptors is associated with an early delay in the modulation of gastric motility by EA at ST36. GABA and L-Glu in the DMV are involved in regulating gastric motility by EA at ST36.

Research perspectives

The results prove that both vagal and sympathetic reflexes are involved in regulating gastric motility by EA at ST36. Future studies should investigate specific transcutaneous stimulation which can regulate gastric motility accurately.