Mediation of thyrotropin-releasing hormone induced gastric motility increases in developing rats.

Centrally administered thyrotropin-releasing hormone (TRH) induces vagally mediated gastrointestinal effects which may be cholinergic, serotonergic or a combination. This study investigated mediation of TRH-stimulated gastric motility in developing rats. A serotonin (5-HT) antagonist (5-HT2, ketanserin or xylamidine; 5-HT3, MDL 72222) or an acetylcholine receptor blocker (atropine) was administered intraperitoneally 30 min prior to intracisternal TRH (5-10 micrograms). The 5-HT-depleting para-chlorophenylalanine (p-CPA) was administered 48 or 72 h prior to TRH. Gastric motility, monitored via extraluminal strain gauge, was not increased with TRH in atropine-pretreated rats. MDL 72222 had a significant age-related effect on TRH-induced gastric motility increases while 5-HT2 antagonists and p-CPA treatment did not. Thus, acetylcholine receptor blockade inhibits TRH-stimulated gastric motility in young and adult rats while 5-HT3 antagonism eliminates the motility response in young (7 and 10 days) rats.