Henke P G, Sullivan R M, Ray A
Department of Psychology, St. Francis Xavier University, Antigonish, N.S., Canada.
Neurosci Lett. 1988 Aug 15;91(1):95-100. doi: 10.1016/0304-3940(88)90255-8.
Bilateral microinjections of thyrotropin-releasing hormone (TRH; 1, 3 and 10 micrograms) into the central nucleus of the amygdala produced a dose-related aggravation of cold restraint-induced gastric ulcers in rats. TRH (10 micrograms) also induced gastric erosions in non-stressed animals. Pretreatment with atropine methyl nitrate attenuated the TRH-induced ulcers in both stress and non-stress situations. TRH (10 micrograms) also antagonized the gastric cytoprotection of intra-amygdalar neurotensin (10 micrograms) and was ineffective in altering the stress ulcer-attenuating effects of dopamine (10 micrograms). Pretreatment with i.p. clozapine, however, prevented the inhibitory effects of dopamine on the TRH-induced aggravation of the gastric stress pathology. The results suggest an interaction of TRH, neurotensin and dopamine in the central amygdalar nucleus during stress, and indicate peripheral cholinergic pathways in the mediation of the ulcerogenic effects of TRH.
向大鼠杏仁核中央核双侧微量注射促甲状腺激素释放激素（TRH；1、3和10微克）会导致与剂量相关的冷束缚诱导胃溃疡加重。TRH（10微克）也会在非应激动物中诱发胃糜烂。用硝酸甲基阿托品预处理可减轻应激和非应激情况下TRH诱导的溃疡。TRH（10微克）也拮抗杏仁核内神经降压素（10微克）的胃细胞保护作用，并且在改变多巴胺（10微克）减轻应激性溃疡的作用方面无效。然而，腹腔注射氯氮平预处理可防止多巴胺对TRH诱导的胃应激病理加重的抑制作用。结果表明在应激期间TRH、神经降压素和多巴胺在杏仁核中央核存在相互作用，并表明外周胆碱能途径在介导TRH的致溃疡作用中起作用。
