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, but few studies exist on how vagovagal and sympathetic reflexes affect EA to regulate gastrointestinal motility.
To study the role of vagovagal and sympathetic reflexes in EA at ST36, as well as the associated receptor subtypes that are involved.
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].
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.
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.
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.