Intracisternal TRH analog increases gastrin release and corpus histidine decarboxylase activity in rats

Author:

Song Min1,Yang Hong1,Walsh John H.1,Ohning Gordon1,Wong Helen1,Taché Yvette1

Affiliation:

1. CURE: Digestive Diseases Research Center, West Los Angeles Veterans Affairs Medical Center, and Digestive Diseases Division, Department of Medicine and Brain Research Institute, University of California, Los Angeles, California 90073

Abstract

Thyrotropin-releasing hormone (TRH) acts in brain stem nuclei to induce vagally mediated stimulation of gastric secretion. The effects of intracisternal injection of the TRH analog RX-77368 on plasma gastrin levels and corpus histidine decarboxylase (HDC) activity were studied in 48-h fasted conscious rats. RX-77368 (25–100 ng) increased plasma gastrin levels by threefold at 30 min, which remained significantly higher than control at 2 and 4 h postinjection. Corpus HDC activity began to increase at 2 h and reached a peak at 4 h postinjection with a 21-fold maximum response observed at 50 ng. Morphological changes in the appearance of corpus HDC-immunoreactive cells correlated well with HDC activity. Pretreatment with gastrin monoclonal antibody completely prevented RX-77368 stimulatory effects on HDC activity. Atropine significantly attenuated gastrin increase at 30 min by 26%. These results indicated that in conscious fasted rats, TRH analog acts in the brain to increase corpus HDC activity in the enterochromaffin-like cells, which involves gastrin release stimulated by central TRH analog.

Publisher

American Physiological Society

Subject

Physiology (medical),Gastroenterology,Hepatology,Physiology

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