Mas-related G protein-coupled receptor D is involved in modulation of murine gastrointestinal motility
| Autor: | Jia Li, Fengyi Wan, Lin Liu, Zongxiang Tang, Lei Lan, Min Xu, Zhudi Zhang |
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| Rok vydání: | 2021 |
| Předmět: |
Agonist
Nutrition and Dietetics Physiology Chemistry medicine.drug_class Colon Motility Ileum General Medicine Pharmacology Receptors G-Protein-Coupled Mice Inbred C57BL Mice medicine.anatomical_structure Dorsal root ganglion In vivo Physiology (medical) Ganglia Spinal medicine Systemic administration Animals Receptor Gastrointestinal Motility Gastrointestinal Transit Ex vivo |
| Zdroj: | Experimental physiologyREFERENCES. 106(12) |
| ISSN: | 1469-445X |
| Popis: | New findings What is the central question of this study? The physiological implication of MrgprD in gastrointestinal motility is unknown. The aim of this study is to assess the effects of MrgprD and its receptor agonists on murine gastrointestinal motility. What is the main finding and its importance? Mrgprd deficiency improves the mouse gastrointestinal motility in vivo but has no effects on the spontaneous contractions of murine intestinal rings ex vivo. The systemic administration of the MrgprD ligand, either β-alanine or alamandine, delays the gastrointestinal transit in vivo and attenuates the spontaneous contractions of the isolated intestinal rings ex vivo. Abstract Mas-related G protein-coupled receptor D (MrgprD) was first identified in sensory neurons of mouse dorsal root ganglion and has been demonstrated to be involved in sensations of pain and itch. Although the expression of MrgprD has been recently found in the gastrointestinal (GI) tract, its physiological role in the GI motility is unknown. To address this question, we used Mrgprd knockout (Mrgprd-/- ) mice and the MrgprD receptor agonists to examine the effects of Mrgprd gene deletion and the MrgprD signaling activation, respectively, on the murine intestinal motility both in vivo and ex vivo. We observed that the deletion of Mrgprd accelerated the transmission of charcoal through the mouse GI tract. But Mrgprd deficiency did not affect the mean amplitudes and the frequencies of the spontaneous contractions in ileum ex vivo. The colonic motor complexes (CMCs) in the proximal and the distal colons were recorded from wild-type (WT) and Mrgprd-/- mice, but their control frequencies were not different. Moreover, in WT mice, the systemic administration of the MrgprD agonist, either β-alanine or alamandine, delayed the GI transit in vivo and suppressed the spontaneous contractions in ileum and the CMCs in colon ex vivo. Our results suggest that MrgprD and its agonist are involved in the modulation of GI motility in mice. This article is protected by copyright. All rights reserved. |
| Databáze: | OpenAIRE |
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