Electroacupuncture at ST36 modulates gastric motility via vagovagal and sympathetic reflexes in rats

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.

Acupuncture at Gastric Back‐Shu and Front‐Mu Acupoints Enhances Gastric Motility via the Inhibition of the Glutamatergic System in the Hippocampus

“…Neurotransmitters, modulators, and pathways of the central nervous system are important factors in the regulation of gastrointestinal motility by EA [32]. e study showed that both GABA and glutamate in the brainstem circuit are involved in the regulation of gastric motility by EA at ST36 [33]. Glutamate is the major excitatory neurotransmitter in the central nervous system and its receptors include both ionotropic receptors and metabotropic receptors.…”

Neuromechanism of acupuncture regulating gastrointestinal motility

“…In addition to the excitement effect, lower extremity acupoints also suggest an inhibitory effect on GI movement, and the inhibitory rate of ST37/LI11 on gastric movement fluctuates between 6.67%–1.33%[ 58 , 59 ]. Moreover, the effect of ST36 on gastric movement is reversed to inhibition after gene knockout of M2 and M3 receptor subtypes[ 45 ], suggesting the involvement of other receptors. This might be caused by activation of the other vagus pathway, the inhibitory non-adrenergic, noncholinergic (NANC) pathway, whose transmitter is nitric oxide (NO) or vasoactive intestinal polypeptide (VIP), to cause smooth muscle relaxation[ 60 ].…”

“…According to a previous study[ 65 ], the abdominal acupoints for gastric motility could be effective within 30 s with a shorter response time, while the acupoint of the hindlimb was effective after 30 s with a longer response time. ST36 showed an excitatory effect in a fast onset manner in sympathectomy rats and β 1&2 knockout mice, suggesting that sympathetic inhibition might be one of the key factors for the delayed onset of ST36 and β1 and β2 receptors may underlie its receptor mechanisms[ 44 , 45 ]. Undoubtedly, the sympathetic pathway is activated by acupoints in the lower limbs; evidence shows that EA at ST36/ST37 increased sympathetic activity in healthy volunteers using a heart rate variability analysis or microneurography evaluation of the left peroneal nerve[ 66 , 67 ].…”

“…EA at PC6 showed no marked change after the injection of L-Glu; however, gastric movement and the parasympathetic nerve firing after injection of GABA were enhanced, indicating that GABA transmission of the DMV underlies the facilitation of EA at PC6 on gastric motility[ 44 ]. EA at ST36[ 45 ] is capable of modulating gastric motility after the injection of L-Glu and GABA, suggesting that both Glu and the GABA receptor in the DMV participate in promoting the gastric motility effect of EA at ST36, i.e ., EA at ST36 and PC6 modulate gastric motility via the vagovagal reflex.…”

Efficacy and safety of Acupuncture for Gastrointestinal Dysfunction after Laparoscopy: study protocol for a randomized controlled trial

“…The regulating effect of acupuncture for gastrointestinal function may be achieved by stimulating nerves, especially vagus nerve. Lu [10] Found that electroacupuncture at ST36 regulated gastric motility in rats through vagus and sympathetic reflex respectively mediated by m2 / 3 and β1 / 2 receptors, and vagus reflex played a major role in this procedure. The results of a research showed that ST36 could stimulate the peroneal nerve, and then transmit the pulse signal to the vagus nerve through the sciatic nerve, release the 1-amino acid decarboxylase and increase the neurotransmitter level [11] .…”