Electroacupuncture at ST36 modulates gastric motility via vagovagal and sympathetic reflexes in rats
Electroacupuncture at ST36 modulates gastric motility via vagovagal and sympathetic reflexes in rats作者机构：Key Laboratory of Acupuncture and Medicine Research of Ministry of Education Nanjing University of Chinese Medicine
出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)
年 卷 期：2019年第25卷第19期
页 面：2315-2326页
核心收录：
基 金：Supported by the National Natural Science Foundation of China,No.81373749 No.81574071,and No.81673883
主 题：Gastric motility Electroacupuncture Vagovagal reflex Sympathetic nerve Rats
摘 要：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 *** To study the role of vagovagal and sympathetic reflexes in EA at ST36, as well as the associated receptor subtypes that are *** 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 receptorknockout(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 tha
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