scholarly journals Neural Mechanism and Possible Role of Inhibition of Gastric Motility Induced by Superior Laryngeal Afferents

2005 ◽  
Vol 30 (Supplement 1) ◽  
pp. i72-i73 ◽  
Author(s):  
M. Kobashi
Keyword(s):  
Gastric Motility ◽  
Neural Mechanism

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.

Evidence against local neural mechanism for intestinal postprandial hyperemia

1983 ◽  
Vol 245 (3) ◽  
pp. H437-H446 ◽  
Author(s):  
R. A. Nyhof ◽  
C. C. Chou
Keyword(s):  
Oxygen Consumption ◽  
Oleic Acid ◽  
Neural Mechanism ◽  
Jejunal Mucosa ◽  
Vasoactive Substances ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Postprandial Hyperemia

The role of local intestinal nerves in the nutrient-induced intestinal hyperemia was investigated in jejunal segments of anesthetized dogs by comparing the hyperemic effect of intraluminal glucose and oleic acid solutions before and after mucosal anesthesia and infusions of methysergide, hexamethonium, and tetrodotoxin. Methysergide, hexamethonium, and tetrodotoxin all failed to alter either the vascular or metabolic responses to luminal placement of glucose or oleic acid. The increases in blood flow and oxygen uptake produced by glucose or oleic acid, however, were blocked or attenuated after exposing the mucosa to dibucaine. The effect was norepinephrine due to an altered vascular response to vasoactive substances as dibucaine did not alter vascular responses to isoproterenol or norepinephrine. Dibucaine, however, inhibited active transport and increased passive transport of glucose across rat intestinal sacs in vitro. Oxygen consumption of the canine jejunal mucosa was also inhibited by dibucaine in vitro. It seems that inhibition of the nutrient-induced intestinal hyperemia by dibucaine is due, at least in part, to its effect on oxygen consumption and glucose transport of the mucosal epithelial cells. Nutrient-induced hyperemia appears not to be neurally mediated but more closely related to metabolism.

scholarly journals Ileal short-chain fatty acids inhibit gastric motility by a humoral pathway

2000 ◽  
Vol 279 (5) ◽  
pp. G925-G930 ◽  
Author(s):  
G. Cuche ◽  
J. C. Cuber ◽  
C. H. Malbert
Keyword(s):  
Gastric Motility ◽  
Short Chain Fatty Acid ◽  
Peptide Yy ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Maximal Amplitude ◽  
Inhibiting Factor ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

The aim of this study was to evaluate the nervous and humoral pathways involved in short-chain fatty acid (SCFA)-induced ileal brake in conscious pigs. The role of extrinsic ileal innervation was evaluated after SCFA infusion in innervated and denervated Babkin's ileal loops, and gastric motility was measured with strain gauges. Peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) concentrations were evaluated in both situations. The possible involvement of absorbed SCFA was tested by using intravenous infusion of acetate. Ileal SCFA infusion in the intact terminal ileum decreased the amplitude of distal and terminal antral contractions (33 ± 1.2 vs. 49 ± 1.2% of the maximal amplitude recorded before infusion) and increased their frequency (1.5 ± 0.11 vs. 1.3 ± 0.10/min). Similar effects were observed during SCFA infusion in ileal innervated and denervated loops (amplitude, 35 ± 1.0 and 34 ± 0.8 vs. 47 ± 1.3 and 43 ± 1.2%; frequency, 1.4 ± 0.07 and 1.6 ± 0.06 vs. 1.1 ± 0.14 and 1.0 ± 0.12/min). Intravenous acetate did not modify the amplitude and frequency of antral contractions. PYY but not GLP-1 concentrations were increased during SCFA infusion in innervated and denervated loops. In conclusion, ileal SCFA inhibit distal gastric motility by a humoral pathway involving the release of an inhibiting factor, which is likely PYY.

scholarly journals When honest people cheat, and cheaters are honest: Cognitive control processes override our moral default

2020 ◽  
Author(s):  
Sebastian P.H. Speer ◽  
Ale Smidts ◽  
Maarten A.S. Boksem
Keyword(s):  
Cognitive Control ◽  
Inferior Frontal Gyrus ◽  
Neural Mechanism ◽  
Cingulate Cortex ◽  
Posterior Cingulate Cortex ◽  
Anterior Cingulate ◽  
Temporoparietal Junction ◽  
Self Image ◽  
Trial Basis

AbstractEvery day, we are faced with the conflict between the temptation to cheat for financial gains and maintaining a positive image of ourselves as being a ‘good person’. While it has been proposed that cognitive control is needed to mediate this conflict between reward and our moral self-image, the exact role of cognitive control in (dis)honesty remains elusive. Here, we identify this role, by investigating the neural mechanism underlying cheating. We developed a novel task which allows for inconspicuously measuring spontaneous cheating on a trial-by-trial basis in the MRI scanner. We found that activity in the Nucleus Accumbens promotes cheating, particularly for individuals who cheat a lot, while a network consisting of Posterior Cingulate Cortex, Temporoparietal Junction and Medial Prefrontal Cortex promotes honesty, particularly in individuals who are generally honest. Finally, activity in areas associated with Cognitive Control (Anterior Cingulate Cortex and Inferior Frontal Gyrus) helped dishonest participants to be honest, whereas it promoted cheating for honest participants. Thus, our results suggest that cognitive control is not needed to be honest or dishonest per se, but that it depends on an individual’s moral default.

Plasticity: Cells, Circuits, Brains, and Behavior

2016 ◽  
Author(s):  
Patricia S. Churchland ◽  
Terrence J. Sejnowski
Keyword(s):  
Nervous System ◽  
Synaptic Plasticity ◽  
Classical Conditioning ◽  
Neuronal Plasticity ◽  
Neural Mechanism ◽  
Synaptic Strength ◽  
Physical Mechanisms ◽  
And Behavior ◽  
The Brain

This chapter examines the physical mechanisms in nervous systems in order to elucidate the structural bases and functional principles of synaptic plasticity. Neuroscientific research on plasticity can be divided into four main streams: the neural mechanism for relatively simple kinds of plasticity, such as classical conditioning or habituation; anatomical and physiological studies of temporal lobe structures, including the hippocampus and the amygdala; study of the development of the visual system; and the relation between the animal's genes and the development of its nervous system. The chapter first considers the role of the mammalian hippocampus in learning and memory before discussing Donald Hebb's views on synaptic plasticity. It then explores the mechanisms underlying neuronal plasticity and those that decrease synaptic strength, the relevance of time with respect to plasticity, and the occurrence of plasticity during the development of the nervous system. It also describes modules, modularity, and networks in the brain.

Role of prostaglandins in regulating gastric motility

1984 ◽  
Vol 247 (2) ◽  
pp. G117-G126 ◽  
Author(s):  
K. M. Sanders
Keyword(s):  
Gastric Emptying ◽  
Gastric Motility ◽  
Motor Performance ◽  
Tonic Contraction ◽  
Frequency Effect ◽  
Dominant Effect ◽  
Proximal Stomach ◽  
Distal Stomach ◽  
Endogenous Prostaglandins

Muscles of the stomach possess the ability to synthesize several prostaglandins. These compounds function as local regulatory agents by influencing the motor performance of the muscle cells. In the distal stomach the dominant effect of endogenous prostaglandins is to decrease the amplitude of contractions and decrease the ability of the muscles to respond to excitatory stimuli. Prostaglandins also have a chronotropic role in the distal stomach, and they are responsible for the frequency effect of gastrin pentapeptide. In the proximal stomach prostaglandins have an opposite role; they promote tonic contraction. Because of the diverse effects of prostaglandins, they probably have complicated effects on gastric motility. In general, emptying of solids should be retarded by endogenous prostaglandins, whereas emptying of fluids may be facilitated by these compounds. Overproduction of prostaglandins may produce abnormal motility patterns and affect gastric emptying. A case of gastric pseudoobstruction apparently involving prostaglandins is discussed.

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