scholarly journals The Neural Mechanism by Which the Dorsal Vagal Complex Mediates the Regulation of the Gastric Motility by Weishu (RN12) and Zhongwan (BL21) Stimulation

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Hao Wang ◽  
Guo-ming Shen ◽  
Wei-jian Liu ◽  
Shun Huang ◽  
Meng-ting Zhang
Keyword(s):  
Gastric Motility ◽  
Gastrointestinal Hormones ◽  
Neural Mechanism ◽  
Neural Mechanisms ◽  
Dorsal Vagal Complex ◽  
Nerve Transection ◽  
Motility Regulation ◽  
Lines Of Evidence ◽  
Stimulation Of

A large number of studies have been conducted to explore the mechanism of Back-Shu and Front-Mu points. While several lines of evidence addressed the acupuncture information of Shu acupoints and Mu acupoints gathering in the spinal cord, whether the convergence is extended to the high centre still remains unclear. The study selected gastric Mu points (RN12) and gastric Shu points (BL21) regulating gastric motility and its central neural mechanisms as the breakthrough point, using the technique of immunochemistry, nuclei lesion, electrophysiology, and nerve transection. Here, we report that gastric motility regulation of gastric Shu and Mu acupoints and their synergistic effect and the signals induced by electroacupuncture (EA) stimulation of acupoints RN12 and RN12 gather in the dorsal vagal complex (DVC), increasing the levels of gastrointestinal hormones in the DVC to regulate gastric motility through the vagus. In sum, our data demonstrate an important role of DVC and vagus in the regulation of gastric motility by EA at gastric Shu and Mu points.

scholarly journals NMDA Receptor-Dependent Synaptic Activity in Dorsal Motor Nucleus of Vagus Mediates the Enhancement of Gastric Motility by Stimulating ST36

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Xinyan Gao ◽  
Yongfa Qiao ◽  
Baohui Jia ◽  
Xianghong Jing ◽  
Bin Cheng ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Gastric Motility ◽  
Low Frequency ◽  
Synaptic Activity ◽  
Motor Nucleus ◽  
Dorsal Motor Nucleus ◽  
Vagal Reflex ◽  
Precise Molecular Mechanism ◽  
Lines Of Evidence

Previous studies have demonstrated the efficacy of electroacupuncture at ST36 for patients with gastrointestinal motility disorders. While several lines of evidence suggest that the effect may involve vagal reflex, the precise molecular mechanism underlying this process still remains unclear. Here we report that the intragastric pressure increase induced by low frequency electric stimulation at ST36 was blocked by AP-5, an antagonist of N-methyl-D-aspartate receptors (NMDARs). Indeed, stimulating ST36 enhanced NMDAR-mediated, but not 2-amino-3-(5-methyl-3-oxo-1,2-oxazol-4-yl)propanoic-acid-(AMPA-) receptor-(AMPAR-) mediated synaptic transmission in gastric-projecting neurons of the dorsal motor nucleus of the vagus (DMV). We also identified that suppression of presynapticμ-opioid receptors may contribute to upregulation of NMDAR-mediated synaptic transmission induced by electroacupuncture at ST36. Furthermore, we determined that the glutamate-receptor-2a-(NR2A-) containing NMDARs are essential for NMDAR-mediated enhancement of gastric motility caused by stimulating ST36. Taken together, our results reveal an important role of NMDA receptors in mediating enhancement of gastric motility induced by stimulating ST36.

Role of adipokines in regulation of colonic motor activity in overweight and obese individuals

2021 ◽  
pp. 48-51
Author(s):  
М. М. Fedorin ◽  
M. A. Livzan ◽  
O. V. Gaus
Keyword(s):  
Literature Search ◽  
Colonic Motility ◽  
Gastrointestinal Hormones ◽  
Colonic Motor ◽  
Motility Regulation ◽  
Colonic Motor Activity ◽  
And Function ◽  
Overweight Or Obesity ◽  
Key Words Colon

The increasing proportion of the population suffering from overweight or obesity is now taking on the character of a pandemic. In the literature, there have begun to appear reports of associations in individuals with impaired colonic motility and a body mass index above 25 kg/m2. The present publication was prepared to systematize data on possible mechanisms of colonic motility disorders in overweight and obese individuals, including through changes in adipokine secretion and function. The literature search was performed in Embase, PubMed, and Google Scholar, using the key words ‘colon motility regulation’, ‘adipokines’, ‘gastrointestinal hormones’, ‘intestinal microbiota’, ‘overweight’, ‘obesity’, ‘visceral fat’.

scholarly journals Effects of Electrical Stimulation at Different Locations in the Central Nucleus of Amygdala on Gastric Motility and Spike Activity

2016 ◽  
pp. 693-700 ◽  
Author(s):  
F. HE ◽  
H.-B. AI
Keyword(s):  
Electrical Stimulation ◽  
Gastric Motility ◽  
Spike Activity ◽  
Central Nucleus ◽  
Motor Nucleus ◽  
Dorsal Vagal Complex ◽  
Motility Index ◽  
Medial Nucleus ◽  
Dorsal Motor Nucleus ◽  
Stimulation Of

The aim of the study was to determine the effects of electrical stimulation of different locations in the central nucleus of amygdala (CNA) on gastric motility and spike activity in dorsal vagal complex. Gastric motility index (GMI) and firing rate (FR) of dorsal vagal complex neurons were measured in adult Wistar rats respectively. Neuronal spikes in dorsal vagal complex (DVC) were recorded extracellularly with single-barrel glass microelectrodes. Each type of responses elicited by electrical stimulation in medial (CEM) and lateral (CEL) subdivisions of CNA were recorded, respectively. GMI was significantly increased after stimulation of CEM (p<0.01), and significantly decreased in response to CEL stimulation (p<0.01). After stimulation of CEM, FR in medial nucleus of the solitary tract (mNST) decreased by 31.6 % (p<0.01) and that in dorsal motor nucleus of the vagus (DMNV) increased by 27.1 % (p<0.01). On the contrary, FR in mNST increased (p<0.01) and that in DMNV decreased in response to CEL stimulation (p<0.05). In conclusions, our findings indicated that different loci of CNA may mediate differential effects on gastric activity via changes in the firing of brainstem neurons controlling gut activity.

Stimulation of Ca(2+)-dependent exocytosis of the sperm acrosome by cAMP acting downstream of phospholipase A2

Reproduction ◽  
2000 ◽  
pp. 57-68 ◽  
Author(s):  
J Garde ◽  
ER Roldan
Keyword(s):  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Phospholipase C ◽  
Phosphodiesterase Inhibitors ◽  
Dibutyryl Camp ◽  
Camp Phosphodiesterase ◽  
Ram Sperm ◽  
Camp Formation ◽  
Stimulation Of

Spermatozoa undergo exocytosis in response to agonists that induce Ca2+ influx and, in turn, activation of phosphoinositidase C, phospholipase C, phospholipase A2, and cAMP formation. Since the role of cAMP downstream of Ca2+ influx is unknown, this study investigated whether cAMP modulates phospholipase C or phospholipase A2 using a ram sperm model stimulated with A23187 and Ca2+. Exposure to dibutyryl-cAMP, phosphodiesterase inhibitors or forskolin resulted in enhancement of exocytosis. However, the effect was not due to stimulation of phospholipase C or phospholipase A2: in spermatozoa prelabelled with [3H]palmitic acid or [14C]arachidonic acid, these reagents did not enhance [3H]diacylglycerol formation or [14C]arachidonic acid release. Spermatozoa were treated with the phospholipase A2 inhibitor aristolochic acid, and dibutyryl-cAMP to test whether cAMP acts downstream of phospholipase A2. Under these conditions, exocytosis did not occur in response to A23187 and Ca2+. However, inclusion of dibutyryl-cAMP and the phospholipase A2 metabolite lysophosphatidylcholine did result in exocytosis (at an extent similar to that seen when cells were treated with A23187/Ca2+ and without the inhibitor). Inclusion of lysophosphatidylcholine alone, without dibutyryl-cAMP, enhanced exocytosis to a lesser extent, demonstrating that cAMP requires a phospholipase A2 metabolite to stimulate the final stages of exocytosis. These results indicate that cAMP may act downstream of phospholipase A2, exerting a regulatory role in the exocytosis triggered by physiological agonists.

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