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National Institute of Mental Health, National Institute of Health (B.H., B.J.H.), National Institute of Child Health and Disease (A.Z.), Basic Neuroscience Program, National Institute of Neurological Disorders and Stroke (É.M.), NIH, Bethesda, Maryland 20892; First Department of Medicine (B.H.), Medical University of Pécs, H-7643 Pécs, Ifjúság u 13, Hungary
Address all correspondence and requests for reprints to: Éva Mezey, BNP/NINDS/NIH, Building 36 Rm 3A17, 9000 Rockville Pike, Bethesda, Maryland 20892. E-mail: mezey{at}codon.nih.gov
Gastrin and histamine both potently stimulate secretion of acid into the gastric lumen. How these agents interact and how their release is controlled is poorly understood. Therefore, we decided to look for histamine in the antral portion of the rat stomach where the gastrin-producing G cells are located. We used immunocytochemical methods to visualize histamine, histidine decarboxylase (HDC, the enzyme that converts histidine to histamine), and the type 1 vesicular monoamine transporter (VMAT1, the protein responsible for moving histamine into vesicles for storage and release). We were surprised to find that histamine, HDC, and VMAT1 were all present in G cells. Our results suggest that G cells synthesize and secrete gastrin and histamine. Whether histamine acts in concert with gastrin to stimulate acid secretion, or functions as an autocrine inhibitor of gastrin release remains to be seen.
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