Poster Presentations by Authors from A‐Z (alphabetical order)

Objective: In the last years a plethora of studies\udaddressed dopamine (DA) as a modulator within the\udenteric nervous system (ENS), controlling gastrointestinal\ud(GI) functions via activation of D1- and D2-like\udreceptors. However, the effective role and functional\udsignificance of DA in the ENS, and the contribution of\udits receptors, are still a matter of debate. Pathological\udalterations of dopaminergic system in the gut may be\udlikely implicated in different motor GI disorders,\udincluding dyspepsia and gastroparesis. Thus, a detailed\udcharacterization of the enteric dopaminergic signalling\udis necessary. The aim of this study was to explore the\udrole of DA in the GI tract, using as model the mouse\uddistal colon.\udMethods: Spontaneous and neurally-evoked mechanical\udactivity of colonic circular muscle strips were investigated\udvia organ bath technique.\udResults: DA (1–300 lM) caused a tetrodotoxin-insensitive\udinhibitory effect on the colonic spontaneous contractions,\udmimicked by bromocriptine, D2-like receptor\udagonist, and antagonized by domperidone, D2-like\udreceptor antagonist. In addition, DA (3 lM) significantly\udreduced the amplitude of neurally-evoked cholinergic\udcontractions, without affecting the direct smooth muscle\udcholinergic contractions elicited by carbachol. DA\udinhibitory effect was mimicked by SKF-38390, D1-like\udreceptor agonist, and antagonized both by SCH-23390,\udD1-like receptor antagonist, and by L-NAME, nitric\udoxide (NO) synthase inhibitor. SCH-23390 per se\udincreased the amplitude of neurally-evoked cholinergic\udcontractions.\udConclusion: DA is a negative modulator of colonic\udmotility via activation of D1- and D2-like receptors.\udAlthough both receptors are available for pharmacological\udrecruitment, only D1-like receptors located on\udenteric neurons appear to be activated by endogenous\udDA. D1-like receptors activation exerts a basal inhibitory\udcontrol on colonic motility, reducing acetylcholine\udrelease from ENS via a NO-dependent pathway