FOOD STIMULATION OF HISTIDINE-DECARBOXYLASE MESSENGER-RNA ABUNDANCE IN RAT GASTRIC FUNDUS

1. Histidine decarboxylase in the enterochromaffin-like cells of the g astric corpus mucosa converts histidine to histamine which in turn sti mulates gastric acid secretion. The control of histidine decarboxylase activity is poorly understood. We have examined how fasting and refee ding influence the abundance of the messenger RNA encoding histidine d ecarboxylase in the gastric corpus of the rat. 2. The polymerase chain reaction was used to generate a probe for detection of histidine deca rboxylase messenger RNA in Northern and slot blots of total RNA from t he gastric corpus of rats fasted for up to 48 h, or fasted and then re fed. A gastrin monoclonal antibody was used to neutralize the action o f endogenous gastrin. 3. Fasting progressively reduced histidine decar boxylase messenger RNA abundance by 3- to 4-fold after 48 h. Refeeding induced a rapid increase in histidine decarboxylase messenger RNA abu ndance which was detectable after 30 min. 4. There was a significant c orrelation between histidine decarboxylase messenger RNA abundance and plasma gastrin. Administration of gastrin antibody inhibited the incr ease in histidine decarboxylase activity after 6 h refeeding, but not after refeeding for 30 min. 5. The results suggest that histamine-medi ated changes in postprandial acid secretion depend on control of histi dine decarboxylase mRNA levels, and that gastrin regulates production of this enzyme in the rat over periods of a few hours.