Role for D1-like and D2-like dopamine receptors in the modulation of intestinal motility in mice

Research output: Contribution to journalMeeting Abstract

Abstract

Objective: In the last years a plethora of studiesaddressed dopamine (DA) as a modulator within theenteric nervous system (ENS), controlling gastrointestinal(GI) functions via activation of D1- and D2-likereceptors. However, the effective role and functionalsignificance of DA in the ENS, and the contribution ofits receptors, are still a matter of debate. Pathologicalalterations of dopaminergic system in the gut may belikely implicated in different motor GI disorders,including dyspepsia and gastroparesis. Thus, a detailedcharacterization of the enteric dopaminergic signallingis necessary. The aim of this study was to explore therole of DA in the GI tract, using as model the mousedistal colon.Methods: Spontaneous and neurally-evoked mechanicalactivity of colonic circular muscle strips were investigatedvia organ bath technique.Results: DA (1–300 lM) caused a tetrodotoxin-insensitiveinhibitory effect on the colonic spontaneous contractions,mimicked by bromocriptine, D2-like receptoragonist, and antagonized by domperidone, D2-likereceptor antagonist. In addition, DA (3 lM) significantlyreduced the amplitude of neurally-evoked cholinergiccontractions, without affecting the direct smooth musclecholinergic contractions elicited by carbachol. DAinhibitory effect was mimicked by SKF-38390, D1-likereceptor agonist, and antagonized both by SCH-23390,D1-like receptor antagonist, and by L-NAME, nitricoxide (NO) synthase inhibitor. SCH-23390 per seincreased the amplitude of neurally-evoked cholinergiccontractions.Conclusion: DA is a negative modulator of colonicmotility via activation of D1- and D2-like receptors.Although both receptors are available for pharmacologicalrecruitment, only D1-like receptors located onenteric neurons appear to be activated by endogenousDA. D1-like receptors activation exerts a basal inhibitorycontrol on colonic motility, reducing acetylcholinerelease from ENS via a NO-dependent pathway.
Original languageEnglish
Pages (from-to)109-109
Number of pages1
JournalNEUROGASTROENTEROLOGY & MOTILITY
Publication statusPublished - 2015

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