Vol. 283, Issue 6, G1310-G1319, December 2002
Cephalic phase of acid secretion involves activation of
medullary TRH receptor subtype 1 in rats
Vicente
Martínez,
María Dolores
Barrachina,
Gordon
Ohning, and
Yvette
Taché
CURE: Digestive Diseases Research Center, Veteran's Affairs
Greater Los Angeles Healthcare System, Department of Medicine, Division
of Digestive Diseases and Brain Research Institute, School of Medicine,
University of California at Los Angeles, Los Angeles, California
90073
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.
gastrin; atropine; nitro-L-arginine methyl ester,
indomethacin; glycine-gastrin antibody; antisense
oligodeoxynucleotides; 2-deoxy-D-glucose; histamine
