Cephalic phase of acid secretion involves activation of medullary TRH receptor subtype 1 in rats

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Abstract
Mechanisms involved in the cephalic phase of gastric acid secretion were studied in awake fasted rats with chronic gastric fistula and exposed to the sight and smell of chow for 30 min. Acid secretion was monitored using constant intragastric perfusion and automatic titration. Sham feeding induced a peak acid response reaching 82 ± 7 μmol/10 min within 20 min compared with the average 22 ± 2 μmol/10 min in controls. The sham-feeding response was abolished by intracisternal pretreatment with the TRH1-receptor antisense oligodeoxynucleotides or subcutaneous injection of atropine, whereas TRH1 mismatch oligodeoxynucleotides had no effect. Serum gastrin was not altered by the sham feeding and increased by refeeding. Gastrin antibody did not block the rise in acid during sham feeding, although the net acid response was reduced by 47% compared with the control group. Glycine-gastrin antibody, indomethacin and nitro-l-arginine methyl ester had no effect. Atropine and gastrin antibody decreased basal acid secretion by 98 and 75%, respectively, whereas all other pretreatments did not. These results indicate that the cholinergic-dependent acid response to sham feeding is mediated by brain medullary TRH1 receptors in rats.