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The role of the hypothalamic peptide thyrotropin-releasing hormone in stress ulcer formation was investigated. In experiment 1, TRH was peripherally administered (10 micrograms/kg) to rats subjected to cold-restraint stress and compared to an inactive peptide; in experiment 2, TRH was administered intracerebroventricularly (0.02, 0.1, and 0.5 microgram/kg) to rats with no adjunctive experimental stress; in experiment 3, TRH antiserum was given intracerebroventricularly to rats subjected to stress and compared to normal rabbit serum. When TRH was administered subcutaneously in rats subjected to stress, it significantly aggravated ulcer formation, and this effect was inhibited by atropine and vagotomy. When administered intracerebroventricularly, TRH alone induced, in a dose-dependent fashion, the formation of gastric ulcers. TRH antiserum infused intracerebroventricularly inhibited ulcer formation induced by cold-restraint stress. In conclusion, TRH seems to play a role in stress ulcer formation, possibly by a cholinergic mediated mechanism.
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