Mediators and enteric nerve pathways controlling gastric emptying

Daniel, E. E.; Tougas, Gervais; Allescher, Hans–Dieter; Vergara, P; Fox-Threlkeld, J. E. T.

doi:10.1007/bf02300374

Cited by 17 publications

(5 citation statements)

References 8 publications

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“…It has been proposed that 5‐HT 3 receptors are located at afferent sensory nerves, and that their activation initiates the chain of excitatory cholinergic mechanisms 21 ,. 37 …”

Section: Discussionmentioning

confidence: 99%

Octreotide enhances the accelerating effect of erythromycin on gastric emptying in healthy subjects

Athanasakis

Chrysos

Zoras

et al. 2002

Aliment Pharmacol Ther

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SUMMARYBackground: Erythromycin exhibits gastrokinetic properties through cholinergic pathways. Reports regarding the action of octreotide on gastric emptying are conflicting. Aim: To assess: (i) the hypothesis that serotonin receptors are involved in the accelerating effect of erythromycin on gastric emptying; and (ii) any modification of the gastrokinetic action of erythromycin induced by octreotide. Subjects and methods: Gastric emptying of a standard meal was estimated in 20 healthy subjects by scintigraphy on three different occasions in a double-blind, placebo-controlled manner and in random order: (i) after placebo; (ii) after 200 mg of intravenous erythromycin; and (iii) after 200 mg of intravenous

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“…It has been proposed that 5‐HT 3 receptors are located at afferent sensory nerves, and that their activation initiates the chain of excitatory cholinergic mechanisms 21 ,. 37 …”

Section: Discussionmentioning

confidence: 99%

Octreotide enhances the accelerating effect of erythromycin on gastric emptying in healthy subjects

Athanasakis

Chrysos

Zoras

et al. 2002

Aliment Pharmacol Ther

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“…It is also critical for host-microbiota interaction and host defense to infection [ 3 , 4 ]. Gastrointestinal motility is physiologically regulated by smooth muscle contractility, that is in turn controlled by extrinsic parasympathetic and sympathetic neurons, intrinsic enteric sensory and motor neurons, and GI hormones [ 5 , 6 , 7 ]. These are influenced by extrinsic factors, such as diet, medications, and infections, as well as intrinsic factors, such as gut–brain communication, inflammatory and degenerative processes, and overstimulation of visceral sensory pathways altering smooth muscle contractility and enteric nervous system function [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Dietary Stimuli, Intestinal Bacteria and Peptide Hormones Regulate Female Drosophila Defecation Rate

et al. 2023

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Peptide hormones control Drosophila gut motility, but the intestinal stimuli and the gene networks coordinating this trait remain poorly defined. Here, we customized an assay to quantify female Drosophila defecation rate as a proxy of intestinal motility. We found that bacterial infection with the human opportunistic bacterial pathogen Pseudomonas aeruginosa (strain PA14) increases defecation rate in wild-type female flies, and we identified specific bacteria of the fly microbiota able to increase defecation rate. In contrast, dietary stress, imposed by either water-only feeding or high ethanol consumption, decreased defecation rate and the expression of enteroendocrine-produced hormones in the fly midgut, such as Diuretic hormone 31 (Dh31). The decrease in defecation due to dietary stress was proportional to the impact of each stressor on fly survival. Furthermore, we exploited the Drosophila Genetic Reference Panel wild type strain collection and identified strains displaying high and low defecation rates. We calculated the narrow-sense heritability of defecation rate to be 91%, indicating that the genetic variance observed using our assay is mostly additive and polygenic in nature. Accordingly, we performed a genome-wide association (GWA) analysis revealing 17 candidate genes linked to defecation rate. Downregulation of four of them (Pmp70, CG11307, meso18E and mub) in either the midgut enteroendocrine cells or in neurons reduced defecation rate and altered the midgut expression of Dh31, that in turn regulates defecation rate via signaling to the visceral muscle. Hence, microbial and dietary stimuli, and Dh31-controlling genes, regulate defecation rate involving signaling within and among neuronal, enteroendocrine, and visceral muscle cells.

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“…Compared to neighbouring regions, the pylorus is supplied with a relatively high density of nerve fibres 2 . It receives excitatory and inhibitory inputs from enteric motor neurones, which are influenced by both extrinsic nerves and hormonal factors 3–6 . The pylorus can be either excited or inhibited by stimulation of vagus nerves 7,8 and is also inhibited by sympathetic stimulation 7 .…”

Section: Introductionmentioning

confidence: 99%

Neuronal control of the pyloric sphincter of the guinea‐pig

Shi

Costa

Brookes

2001

Neurogastroenterology Motil

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The pyloric sphincter (PS) controls gastric emptying and prevents the reflux of duodenal content into the stomach. Neuronal pathways and reflexes controlling the guinea-pig PS were physiologically investigated in isolated preparations. Simultaneous intracellular or extracellular and tension recordings from PS circular muscle with electrical and stretch stimulation were used. Electrical stimulation evoked an initial small contraction followed by a relaxation with a corresponding inhibitory junction potential (IJP) then a second large contraction with a corresponding excitatory junction potential (EJP). Hyoscine (1 micromol L-1) blocked the first contraction, and reduced the second contraction and EJP by 52.5% and 61%, respectively. These responses were further reduced by the NK2 antagonist, MEN10627 (1 micromol L-1), and the NK1 antagonist, SR140333 (1 micromol L-1). N-nitro-L-arginine (100 micro;mol L-1) and apamin (0.5 micromol L-1) blocked the relaxation and the IJP. Duodenal electrical stimulation evoked an EJP, whereas antral stimulation evoked an IJP followed by a small EJP. All were blocked by hexamethonium (100 micromol L-1). Duodenal stretch evoked tetrodotoxin-sensitive reflex contractions and membrane depolarization with action potentials in the PS. Thus, PS enteric motor neurones receive inputs from the duodenum and the stomach. There are stretch-sensitive ascending excitatory reflex pathways from the duodenum to the PS.

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Mediators and enteric nerve pathways controlling gastric emptying

Cited by 17 publications

References 8 publications

Octreotide enhances the accelerating effect of erythromycin on gastric emptying in healthy subjects

Octreotide enhances the accelerating effect of erythromycin on gastric emptying in healthy subjects

Dietary Stimuli, Intestinal Bacteria and Peptide Hormones Regulate Female Drosophila Defecation Rate

Neuronal control of the pyloric sphincter of the guinea‐pig

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