In fish, cholecystokinin (CCK) has been involved in gastrointestinal regulation, with effects being reported on gut motility, gallbladdercontraction and gastric and pancreatic secretion. In the present study, goldfish gut was used to characterize the in vitro effect of CCK on gastrointestinal motility in an organ bath system. The amplitude and force of the smooth muscle contractions were recorded. Our results showed a concentration-dependent contraction induced by CCK, which was maintained in absence of extracellular calcium, although the EC50 increased. The CCK-induced contraction was not inhibited in the presence of atropine (100 ?M), tetrodotoxin (1 ?M), proglumide (1 mM), or L-365,260 (1 ?M) receptor antagonists. Only a CCK-A receptor antagonist, devazepide (1 ?M), reduced the CCK-induced contraction by 30%. Our results indicate that the contractile effect of CCK in goldfish gut is mediated through specific receptors located in muscle. More studies are necessary in order to indentify the CCK receptor subtypes involved in fish intestinal motility.
