Gv. Ohning et al., IMMUNOLOCALIZATION OF GASTRIN-DEPENDENT HISTIDINE-DECARBOXYLASE ACTIVITY IN RAT GASTRIC-MUCOSA DURING FEEDING, American journal of physiology: Gastrointestinal and liver physiology, 38(4), 1998, pp. 660-667
The localization of histidine decarboxylase (HDC) activity; in the ent
erochromaffin-like (ECL) cells of the oxyntic mucosa was studied durin
g fasting and refeeding using monoclonal (CURE no. 44178) and polyclon
al (CURE no. 94211) antibodies directed against the COOH terminus of H
DC (HDC-CT). Changes in HDC immunostaining were correlated with mucosa
l HDC enzyme activity. Immunoneutralization of circulating gastrin and
atropine treatment during refeeding were used to determine the relati
ve importance of gastrin and cholinergic mechanisms in the regulation
of HDC activity and immunostaining. Fasting caused a rapid reduction i
n the number of ECL cells immunostaining for HDC that was correlated w
ith an almost complete loss of mucosal HDC enzyme activity Refeeding r
estored both HDC immunostaining and enzyme activity within 2-4 h, and
this response was inhibited by gastrin immunoneutralization but not by
atropine treatment. Immunostaining was uniformly decreased and restor
ed in the lower half of the oxyntic mucosa, which corresponds to the p
redominant area of ECL cells in the gastric gland. Histamine immunosta
ining and mucosal histamine content were not significantly changed dur
ing fasting and refeeding or by gastrin antibody and/or atropine treat
ment during refeeding These findings indicate that HDC activity correl
ates with HDC-CT immunostaining and that both HDC activity and HDC-CT
immunostaining are regulated by gastrin during refeeding.