The role of serotonin in the control of esophageal sensitivity assessed by multimodal stimulation in health.


Journal

Neurogastroenterology and motility
ISSN: 1365-2982
Titre abrégé: Neurogastroenterol Motil
Pays: England
ID NLM: 9432572

Informations de publication

Date de publication:
03 2021
Historique:
received: 22 05 2020
revised: 22 10 2020
accepted: 17 11 2020
pubmed: 7 12 2020
medline: 1 12 2021
entrez: 6 12 2020
Statut: ppublish

Résumé

Esophageal hypersensitivity is considered an important pathophysiological mechanism in refractory gastroesophageal reflux disease (GERD) patients. Serotonin (5-HT) plays an important role in the regulation of GI (gastrointestinal) secretion, motility and sensitivity. Previous studies found that altered 5-HT availability has no clear effects on esophageal/GI sensations. Our aim was therefore to investigate the role of 5-HT in esophageal sensitivity in healthy volunteers (HV). Esophageal sensitivity to thermal, mechanical, electrical, and chemical stimuli was assessed in 3 different placebo-controlled studies. In the first study, the effect of citalopram (40 mg; 5-HT reuptake inhibitor; intravenous) was investigated (n = 14). In the second study, the effect of buspirone (20 mg; 5HT1A agonist; oral) was investigated (n = 10). In the third study, acute tryptophan depletion (ATD) was used to decrease 5-HT levels to investigate the effect of reduced 5-HT availability on esophageal sensitivity (n = 15). No difference was observed in esophageal sensitivity after the administration of citalopram or buspirone (all p > 0.06). In contrast, pain perception threshold to chemical stimulation was increased after ATD (p = 0.017, Cohen's d+ = 0.67). No effect was found on the first perception or pain tolerance threshold. ATD had no influence on esophageal sensitivity to thermal, mechanical, and electrical stimulation compared with placebo. ATD, which induces 5-HT depletion, significantly decreased pain perception threshold during chemical stimulation, without affecting sensitivity to mechanical, thermal, or electrical stimulation. These findings confirm the involvement of 5-HT in the control of esophageal acid sensitivity, but identifying the receptors involved requires more ligands and studies.

Sections du résumé

BACKGROUND
Esophageal hypersensitivity is considered an important pathophysiological mechanism in refractory gastroesophageal reflux disease (GERD) patients. Serotonin (5-HT) plays an important role in the regulation of GI (gastrointestinal) secretion, motility and sensitivity. Previous studies found that altered 5-HT availability has no clear effects on esophageal/GI sensations. Our aim was therefore to investigate the role of 5-HT in esophageal sensitivity in healthy volunteers (HV).
METHODS
Esophageal sensitivity to thermal, mechanical, electrical, and chemical stimuli was assessed in 3 different placebo-controlled studies. In the first study, the effect of citalopram (40 mg; 5-HT reuptake inhibitor; intravenous) was investigated (n = 14). In the second study, the effect of buspirone (20 mg; 5HT1A agonist; oral) was investigated (n = 10). In the third study, acute tryptophan depletion (ATD) was used to decrease 5-HT levels to investigate the effect of reduced 5-HT availability on esophageal sensitivity (n = 15).
KEY RESULTS
No difference was observed in esophageal sensitivity after the administration of citalopram or buspirone (all p > 0.06). In contrast, pain perception threshold to chemical stimulation was increased after ATD (p = 0.017, Cohen's d+ = 0.67). No effect was found on the first perception or pain tolerance threshold. ATD had no influence on esophageal sensitivity to thermal, mechanical, and electrical stimulation compared with placebo.
CONCLUSIONS AND INFERENCES
ATD, which induces 5-HT depletion, significantly decreased pain perception threshold during chemical stimulation, without affecting sensitivity to mechanical, thermal, or electrical stimulation. These findings confirm the involvement of 5-HT in the control of esophageal acid sensitivity, but identifying the receptors involved requires more ligands and studies.

Identifiants

pubmed: 33280212
doi: 10.1111/nmo.14057
doi:

Substances chimiques

Serotonin Receptor Agonists 0
Serotonin Uptake Inhibitors 0
Citalopram 0DHU5B8D6V
Serotonin 333DO1RDJY
Tryptophan 8DUH1N11BX
Buspirone TK65WKS8HL

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e14057

Informations de copyright

© 2020 John Wiley & Sons Ltd.

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Auteurs

Charlotte Broers (C)

Translational Research Centre for Gastrointestinal Disorders, University of Leuven, Leuven, Belgium.

Annelies Geeraerts (A)

Translational Research Centre for Gastrointestinal Disorders, University of Leuven, Leuven, Belgium.

Veerle Boecxstaens (V)

Translational Research Centre for Gastrointestinal Disorders, University of Leuven, Leuven, Belgium.

Brecht Van Houtte (B)

Translational Research Centre for Gastrointestinal Disorders, University of Leuven, Leuven, Belgium.

Hannelore Geysen (H)

Translational Research Centre for Gastrointestinal Disorders, University of Leuven, Leuven, Belgium.

Nele Peersman (N)

Clinical Department of Laboratory Medicine, University Hospital Leuven, Leuven, Belgium.

Pieter Vermeersch (P)

Clinical Department of Laboratory Medicine, University Hospital Leuven, Leuven, Belgium.

Tim Vanuytsel (T)

Translational Research Centre for Gastrointestinal Disorders, University of Leuven, Leuven, Belgium.

Jan Tack (J)

Translational Research Centre for Gastrointestinal Disorders, University of Leuven, Leuven, Belgium.

Ans Pauwels (A)

Translational Research Centre for Gastrointestinal Disorders, University of Leuven, Leuven, Belgium.

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