scholarly journals Gentle Manual Acupuncture Could Better Regulate Gastric Motility and Vagal Afferent Nerve Discharge of Rats with Gastric Hypomotility

2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Yangyang Liu ◽  
Yang Bai ◽  
Yue Pan ◽  
Zhifang Xu ◽  
Yuxin Fang ◽  
...  
Keyword(s):  
Gastric Motility ◽  
Underlying Mechanism ◽  
Afferent Nerve ◽  
Manual Acupuncture ◽  
Intensity Effect ◽  
Afferent Nerves ◽  
Strong Stimulation ◽  
Vagal Afferent ◽  
Acupuncture Effects ◽  
Nerve Discharge

The variation of stimulus intensity of manual acupuncture (MA) may produce diverse acupuncture effects. However, the intensity-effect relationship and the underlying mechanism of MA are still elusive. In this study, the effects of MA regulation of gastric motility were investigated after lifting-thrusting MA treatment with four different frequencies (1 Hz, 2 Hz, 3 Hz, and 4 Hz) at ST36. The experiments were conducted on rats with gastric hypomotility caused by atropine. The results showed that the gastric motility amplitude decreased after atropine injection, while the treatment of four types of MA affected the gastric motility amplitude in varying degrees. Specifically, 2 Hz MA exhibited the most effective results, while 4 Hz MA had the least effect; the effects of 1 Hz MA and 3 Hz MA were between the effects induced with 2 Hz and 4 Hz. Furthermore, the response of gastric vagal afferent nerve discharge and gastric motility was examined after MA treatment with frequencies of 2 Hz and 4 Hz, respectively, on ST36 in order to elucidate the mechanism of MA regulation of gastric motility. The results showed that 2 Hz MA was able to increase the amplitude of gastric motility and discharge frequency of gastric vagal afferent nerves, while 4 Hz MA exhibited seldom effects. These findings suggest that gentle MA (2 Hz) has more stimulating effects than strong stimulation with MA (4 Hz) on gastric hypomotility. In addition, gastric motility regulated by MA was associated with vagal afferent nerve activation.

scholarly journals GABA signaling in the nucleus tractus solitarius sets the level of activity in dorsal motor nucleus of the vagus cholinergic neurons in the vagovagal circuit

2009 ◽  
Vol 296 (1) ◽  
pp. G101-G111 ◽  
Author(s):  
Melissa A. Herman ◽  
Maureen T. Cruz ◽  
Niaz Sahibzada ◽  
Joseph Verbalis ◽  
Richard A. Gillis
Keyword(s):  
Gastric Motility ◽  
Kynurenic Acid ◽  
Nucleus Tractus Solitarius ◽  
Afferent Nerve ◽  
Projection Neurons ◽  
Motor Nucleus ◽  
Nerve Terminals ◽  
Receptor Blockade ◽  
Dorsal Motor Nucleus ◽  
Vagal Afferent

It has been proposed that there is an “apparent monosynaptic” connection between gastric vagal afferent nerve terminals and inhibitory projection neurons in the nucleus tractus solitarius (NTS) and that two efferent parallel pathways from the dorsal motor nucleus of the vagus (DMV) influence peripheral organs associated with these reflexes ( 6 ). The purpose of our study was to verify the validity of these views as they relate to basal control of gastric motility. To test the validity of a direct connection of vagal afferent terminals (known to release l-glutamate) directly impacting second-order projection neurons, we evaluated the effect of GABAA receptor blockade in the area of the medial subnucleus of the tractus solitarius (mNTS) on gastric motility. Microinjection of bicuculline methiodide into the mNTS produced robust decreases in gastric motility (−1.6 ± 0.2 mmHg, P < 0.05, n = 23), which were prevented by cervical vagotomy and by pretreatment with kynurenic acid microinjected into the mNTS. Kynurenic acid per se had no effect on gastric motility. However, after GABAA receptor blockade in the mNTS, kynurenic acid produced a robust increase in gastric motility. To test for the contribution of two parallel efferent DMV pathways, we assessed the effect of either intravenous atropine methylbromide or NG-nitro-l-arginine methyl ester on baseline motility and on decreases in gastric motility induced by GABAA receptor blockade in the mNTS. Only atropine methylbromide altered baseline motility and prevented the effects of GABAA receptor blockade on gastric motility. Our data demonstrate the presence of intra-NTS GABAergic signaling between the vagal afferent nerve terminals and inhibitory projection neurons in the NTS and that the cholinergic-cholinergic excitatory pathway comprises the functionally relevant efferent arm of the vagovagal circuit.

Secretin inhibits vagal afferent nerve discharge in response to gastric distension in rats

2000 ◽  
Vol 118 (4) ◽  
pp. A840
Author(s):  
Je Lu ◽  
Zong-Seng Huang ◽  
James P. Li ◽  
Ying Zhao ◽  
William Y. Chey
Keyword(s):  
Afferent Nerve ◽  
Gastric Distension ◽  
Vagal Afferent ◽  
Nerve Discharge

Effects of bilateral vagal cold block on vasopressin in conscious dogs

1984 ◽  
Vol 246 (4) ◽  
pp. R566-R569
Author(s):  
V. S. Bishop ◽  
M. D. Thames ◽  
P. G. Schmid
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Afferent Nerve ◽  
Vagal Afferents ◽  
Inhibitory Influence ◽  
Conscious Dog ◽  
Afferent Nerves ◽  
Vagal Afferent ◽  
Plasma Arginine

Bilateral vagal cold block was used to interrupt afferent nerve traffic in the cervical vagi and thus to determine the tonic inhibitory influence of vagal afferents on plasma arginine vasopressin (AVP) concentrations in the conscious dog. Experiments were performed in conscious aortic baroreceptor-denervated dogs with carotid baroreflexes intact or with sinoaortic denervation. In the presence of intact carotid baroreflexes (n = 11) vagal cold block significantly increased arterial pressure (99 +/- 5 to 120 +/- 8 mmHg), heart rate (98 +/- 2 to 168 +/- 11 beats/min), and AVP (2.9 +/- 0.6 to 6.7 +/- 1.3 microU/ml). Chronic sinoaortic denervation did not significantly alter plasma AVP (4.4 +/- 1.0 microU/ml). However, vagal cold block in these totally denervated animals caused a significantly greater increase in arterial pressure (116 +/- 7 to 167 +/- 7 mmHg) and plasma AVP (4.4 +/- 1 to 33.4 +/- 4.8 microU/ml) compared with the responses observed in dogs with intact carotid baroreflexes. These results indicate that vagal afferent nerves exert a significant tonic inhibitory influence on the secretion of AVP in the conscious aortic baroreceptor-denervated dogs as well as in dogs with sinoaortic denervation.

Vagal modulation of intestinal afferent sensitivity to systemic LPS in the rat

2007 ◽  
Vol 292 (5) ◽  
pp. G1213-G1220 ◽  
Author(s):  
C. Y. Liu ◽  
M. H. Mueller ◽  
D. Grundy ◽  
M. E. Kreis
Keyword(s):  
Systemic Blood Pressure ◽  
Feedback Mechanism ◽  
Afferent Nerve ◽  
Vagal Afferents ◽  
Partial Recovery ◽  
Before And After ◽  
The Central Nervous System ◽  
Vagal Afferent ◽  
Nerve Discharge

The central nervous system modulates inflammation in the gastrointestinal tract via efferent vagal pathways. We hypothesized that these vagal efferents receive synaptic input from vagal afferents, representing an autonomic feedback mechanism. The consequence of this vagovagal reflex for afferent signal generation in response to LPS was examined in the present study. Different modifications of the vagal innervation or sham procedures were performed in anesthetized rats. Extracellular mesenteric afferent nerve discharge and systemic blood pressure were recorded in vivo before and after systemic administration of LPS (6 mg/kg iv). Mesenteric afferent nerve discharge increased dramatically following LPS, which was unchanged when vagal efferent traffic was eliminated by acute vagotomy. In chronically vagotomized animals, to eliminate both vagal afferent and efferent traffic, the increase in afferent firing 3.5 min after LPS was reduced to 3.2 ± 2.5 impulses/s above baseline compared with 42.2 ± 2.0 impulses/s in controls ( P < 0.001). A similar effect was observed following perivagal capsaicin, which was used to eliminate vagal afferent traffic only. LPS also caused a transient hypotension (<10 min), a partial recovery, and then persistent hypertension that was exacerbated by all three procedures. Mechanosensitivity was increased 15 min following LPS but had recovered at 30 min in all subgroups except for the chronic vagotomy group. In conclusion, discharge in capsaicin-sensitive mesenteric vagal afferents is augmented following systemic LPS. This activity, through a vagovagal pathway, helps to attenuate the effects of septic shock. The persistent hypersensitivity to mechanical stimulation after chronic vagal denervation suggests that the vagus exerts a regulatory influence on spinal afferent sensitization following LPS.

Duodenal acid-induced gastric relaxation is mediated by multiple pathways

1999 ◽  
Vol 276 (6) ◽  
pp. G1501-G1506 ◽  
Author(s):  
Yuan-Xu Lu ◽  
Chung Owyang
Keyword(s):  
Gastric Motility ◽  
No Reduction ◽  
Direct Action ◽  
Intragastric Pressure ◽  
Afferent Pathways ◽  
Serotonin Antagonist ◽  
Intraduodenal Infusion ◽  
Rate Dependent ◽  
Vagal Afferent

In this study, we used an in vivo anesthetized rat model to investigate the mechanisms responsible for duodenal acid-induced inhibition of gastric motility. Intraduodenal infusion of HCl produced a rate-dependent decrease in intragastric pressure. Infusion of HCl at 2 ml/h produced a physiological plasma secretin level and elicited a decrease in intragastric pressure of 3.0 ± 0.2 cmH20. Infusion of rabbit secretin antiserum reduced the acid-induced inhibition of gastric motility by 85 ± 5%, suggesting mediation mainly by endogenous secretin. Administration of the cholecystokinin (CCK)-A antagonist MK-329 caused only a modest 10 ± 3% reduction in gastric relaxation, whereas the serotonin antagonist ICS-205930 had no effect. In contrast, immunoneutralization with the secretin antibody caused only a 15% reduction in the relaxation evoked by a higher rate of HCl infusion (3 ml/h), whereas MK-329 and ICS-205930 caused a 20 ± 4% reduction and no reduction, respectively. Bilateral truncal vagotomy or perivagal application of capsaicin completely abolished gastric relaxation in response to low rates (1–2 ml/h) of 0.1 N HCl infusion but only partially affected gastric relaxation in response to a higher infusion rate (3 ml/h). These observations indicate that multiple pathways mediate the duodenal acid-induced inhibition of gastric motility. At low rates of HCl infusion, gastric relaxation is mediated primarily by endogenous secretin, which acts through vagal afferent pathways. At higher rates of HCl infusion, gastric relaxation is mediated by endogenous secretin, CCK, and possibly by the direct action of HCl on vagal afferent pathways or yet unidentified neuropathways.

scholarly journals Nervous rhythm arising from rivalry of antagonistic reflexes: Reflex stepping as outcome of double reciprocal innervation

1913 ◽  
Vol 86 (587) ◽  
pp. 233-261 ◽  
Keyword(s):  
Afferent Nerve ◽  
The Other ◽  
Present Communication ◽  
Simultaneous Stimulation ◽  
Afferent Nerves ◽  
Wide Range ◽  
Contralateral Muscle ◽  
Stimulation Of

The observations with which the present communication deals were met with in experiments continuing those on reciprocal innervation of symmetrical muscles. In my previous paper on that subject it had been reported that in regard to symmetrical extensors of the knee the ratio borne by intensity of the ipsilateral inhibition to the contralateral excitation is such that with equal stimuli to right and left symmetrical afferent nerves there is inhibitory suppression of contraction in both the muscles. In other words, under double reciprocal innervation the ipsilateral inhibition by each nerve completely overcomes the contralateral excitation of the other. It was shown that this mutual suppression holds over a wide range of the scale of intensities of stimulation. It was also shown that with quite weak stimuli a simultaneous stimulation of both nerves, stimuli being equal in intensity, often results in concurrent contraction of both muscles. Indeed, with quite weak stimuli, the effect of stimulation of each afferent nerve by itself is, in the decerebrate preparation, usually contraction of the ipsilateral as well as of the contralateral muscle. This being so, it is evident that at some point in the scale of intensities of stimulation there should be a place below which contralateral excitation is stronger than ipsilateral inhibition, whereas above it ipsilateral inhibition is stronger than contralateral excitation.

scholarly journals A102 MONOSODIUM GLUTAMATE INCREASES VISCERAL SENSITIVITY IN A MURINE MODEL OF IRRITABLE BOWEL SYNDROME

2020 ◽  
Vol 3 (Supplement_1) ◽  
pp. 118-119
Author(s):  
B J Brant ◽  
Y Yu ◽  
A E Lomax ◽  
S Vanner ◽  
C J Tuck
Keyword(s):  
Irritable Bowel Syndrome ◽  
Murine Model ◽  
Ex Vivo ◽  
Monosodium Glutamate ◽  
Afferent Nerve ◽  
Nerve Terminals ◽  
Visceral Sensitivity ◽  
Clinical Model ◽  
Afferent Nerves ◽  
Irritable Bowel

Abstract Background Over 70% of patients suffering from symptoms of the irritable bowel syndrome (IBS) report that food is the most common trigger. Patients have identified that monosodium glutamate (MSG) is one food component that they suspect can trigger symptoms, but this remains unproven. As a first step towards establishing a potential role, we sought to examine whether there was a plausible mechanism of how MSG ingestion could underlie exaggerated pain signaling in IBS. Aims To examine the effects of MSG on visceral sensitivity in a murine model of IBS. Methods Balb/c mice were subjected to 6-days of water-avoidance stress (WAS) to create a pre-clinical model for IBS. To assess changes in visceral afferent nerve sensitivity in control and WAS mice, responses to ramp distension (0–60 mmHg), in the absence and presence 10 μM MSG perfused into the intestinal lumen (concentration based on diet analysis of MSG human ingestion), were recorded from afferent nerves innervating the jejunum ex vivo. To quantify these responses, the baseline firing frequency (spikes/second) was subtracted from the maximum response at each distending pressure. The relative distension response was calculated as a percentage of the control distension response (absence of MSG) (Figure 1). Jejunal preparations from the same WAS-treated mice were also used to measure ex vivo changes in mucosal permeability to MSG using Ussing chambers. We also ran the same distension protocol; however, we applied 10 μM MSG directly to the organ bath outside intestine obtained from control mice. This direct application would allow the MSG to have direct access to the nerve terminals without having to traverse the mucosa. Results The intraluminal administration of 10 μM MSG significantly increased afferent nerve sensitivity in WAS-treated jejunum but not controls. This response was significantly greater (23%) at pressures between 40 and 60 mmHg (p&lt;0.01) (Figure 1). WAS-treated mouse jejunum was also significantly more permeable to MSG (p&lt;0.05). Furthermore, the application of 10 μM MSG directly to the bath containing healthy jejunum significantly increased by 25% the sensitivity of afferent nerves specifically at 60 mmHg (p&lt;0.01). Conclusions Our findings demonstrate that MSG increases visceral sensitivity to distension in our pre-clinical model of IBS. The increased permeability to MSG in WAS tissue and increased distension response in healthy control tissue when MSG is applied directly to the bath rather than intraluminally, suggests that MSG signals to the immune compartment or directly to the afferent nerve terminals. These findings support the rationale for future in vivo studies with this model to further clarify the mechanism. Funding Agencies CCC, CIHR

Inhibition of spinal afferent nerve-mediated gastric hyperemia by nicotine: role of ganglionic blockade

1993 ◽  
Vol 264 (4) ◽  
pp. H1087-H1092
Author(s):  
F. W. Leung
Keyword(s):  
Blood Flow ◽  
Afferent Nerve ◽  
Gastric Blood Flow ◽  
Doppler Flowmetry ◽  
Afferent Nerves ◽  
Vasodilatory Effect ◽  
Blocking Property ◽  
Intravenous Nicotine ◽  
Ganglionic Blocking ◽  
Stimulation Of

The hypothesis that intravenous nicotine modulates gastric spinal afferent nerve function by its ganglionic-blocking property is tested. Stimulation of the gastric spinal afferent nerves in anesthetized rats is accomplished by intragastric capsaicin irrigation. Gastric blood flow is monitored by laser-Doppler flowmetry. The increase in gastric blood flow during intragastric capsaicin irrigation is significantly reduced by 4 and 40 micrograms.kg-1.min-1 of intravenous nicotine. The inhibition appears to be specific for the spinal afferent nerves as the increase in gastric blood flow induced by electrical stimulation of the vagal afferent nerves is unaltered by these doses of intravenous nicotine. A ganglionic-blocking dose (10 mg/kg) of intraperitoneal hexamethonium also significantly attenuates the gastric vasodilatory effect of intragastric capsaicin. Intravenous nicotine (40 micrograms.kg-1.min-1) combined with intraperitoneal hexamethonium (10 mg/kg) completely abolishes the gastric vasodilatory effect of intragastric capsaicin. These data suggest that intravenous nicotine offers a specific inhibition of the gastric spinal afferent nerve-mediated hyperemia, possibly as a consequence of its ganglionic-blocking property.

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