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Data sharing statement: No additional unpublished data are available.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
Processing time: 81 Days and 21.6 Hours
Abstract
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, but few studies exist on how vagovagal and sympathetic reflexes affect EA to regulate gastrointestinal motility.

AIM

To study the role of vagovagal and sympathetic reflexes in EA at ST36, as well as the associated receptor subtypes that are involved.

METHODS

Gastric motility was measured with a manometric balloon placed in the gastric antrum area in anesthetized animals. The peripheral nervous discharge was measured using a platinum electrode hooking the vagus or greater splanchnic nerve, and the central nervous discharge was measured with a glass microelectrode in the dorsal motor nucleus of the vagus (DMV). The effects and mechanisms of EA at ST36 were explored in male Sprague-Dawley rats which were divided in to 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].

RESULTS

EA at ST36 promoted gastric motility during 30-120 s. During EA, both vagus and sympathetic nerve discharges increased, with a much higher frequency of vagus nerve discharge than sympathetic discharge. The gastric motility mediated by EA at ST36 was interdicted by vagotomy. However, gastric motility mediated by EA at ST36 was increased during 0-120 s by sympathectomy, which eliminated the delay effect of EA during 0-30 s, but it was lower than the control group during 30-120 s. Using gene knockout mice and their wild-type controls to explore the receptor mechanisms, we found that 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 DMV. Microinjection of L-Glu into the DMV increased gastric motility, while EA at ST36 decreased gastric motility during 0-60 s, and promoted gastric motility during 60-120 s. Injection of GABA reduced or increased gastric motility, and reduced the promoting gastric motility effect of EA at ST36.

CONCLUSION

These data suggest that 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 modulation of gastric motility by EA at ST36.

Keywords: Gastric motility; Electroacupuncture; Vagovagal reflex; Sympathetic nerve; Rats

Core tip: In this study, we measured intragastric pressure to observe the effect of electroacupuncture (EA) at ST36 on gastric motility at different time intervals. The role of the peripheral autonomic nervous system in EA was determined using the vagus nerve and splanchnic nerve severance model, as well as by detecting peripheral autonomic nerve discharge. M2/3 and β1/2 receptor knockout mouse models were further used to identify autonomic receptor subtypes specifically involved in the regulation of gastric motility. Finally, we studied the role of brainstem neurocircuits during EA at ST36 by detecting the dorsal motor nucleus of the vagus (DMV) neuron discharge and the effect of microinjection of γ-aminobutyric acid and glutamate to the DMV. Using these approaches, the role of vagovagal and sympathetic reflexes in regulating gastric motility by EA at ST36 was determined.