Published online May 21, 2019. doi: 10.3748/wjg.v25.i19.2315
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
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.
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.
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.
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].
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.
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.
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.