Bond E F, Heitkemper M M, Gruver M K
Department of Physiological Nursing, University of Washington, Seattle 98195.
Eur J Pharmacol. 1992 Jul 7;217(2-3):127-35. doi: 10.1016/0014-2999(92)90831-n.
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.
中枢给予促甲状腺激素释放激素（TRH）可诱发由迷走神经介导的胃肠道效应，这些效应可能是胆碱能、5-羟色胺能或两者兼有的。本研究调查了TRH刺激发育中大鼠胃动力的介导机制。在脑池内给予TRH（5 - 10微克）前30分钟，腹腔注射5-羟色胺（5-HT）拮抗剂（5-HT2，酮色林或赛拉米定；5-HT3，MDL 72222）或乙酰胆碱受体阻滞剂（阿托品）。在给予TRH前48或72小时给予5-HT耗竭剂对氯苯丙氨酸（p-CPA）。通过腔外应变仪监测胃动力，在阿托品预处理的大鼠中，TRH未增加胃动力。MDL 72222对TRH诱导的胃动力增加有显著的年龄相关效应，而5-HT2拮抗剂和p-CPA处理则没有。因此，乙酰胆碱受体阻断抑制幼龄和成年大鼠中TRH刺激的胃动力，而5-HT3拮抗作用消除幼龄（7和10日龄）大鼠中的动力反应。
