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Am J Physiol Gastrointest Liver Physiol 279: G677-G682, 2000;
0193-1857/00 $5.00
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Vol. 279, Issue 4, G677-G682, October 2000

Effects of gamma -aminobutyric acid on secretagogue-induced exocrine secretion of isolated, perfused rat pancreas

Hyung Seo Park2 and Hyoung Jin Park1

1 Department of Physiology, College of Medicine, Hallym University, Chunchon, Kangwon-Do 200-702; and 2 Department of Physiology, College of Medicine, Konyang University, Nonsan, Chungnam-Do 320-711, Korea

Because GABA and its related enzymes have been determined in beta -cells of pancreas islets, effects of GABA on pancreatic exocrine secretion were investigated in the isolated, perfused rat pancreas. GABA, given intra-arterially at concentrations of 3, 10, 30, and 100 µM, did not exert any influence on spontaneous or secretin (12 pM)-induced pancreatic exocrine secretion. However, GABA further elevated CCK (10 pM)-, gastrin-releasing peptide (100 pM)-, or electrical field stimulation-induced pancreatic secretions of fluid and amylase dose dependently. The GABA (30 µM)-enhanced CCK-induced pancreatic secretions were completely blocked by bicuculline (10 µM), a GABAA receptor antagonist, but were not affected by saclofen (10 µM), a GABAB receptor antagonist. The enhancing effects of GABA (30 µM) on CCK-induced pancreatic secretions were not changed by tetrodotoxin (1 µM) but were partially reduced by cyclo-(7-aminoheptanonyl-Phe-D-Trp-Lys-Thr[BZL]) (10 nM), a somatostatin antagonist. In conclusion, GABA enhances pancreatic exocrine secretion induced by secretagogues, which predominantly induce enzyme secretion, via GABAA receptors in the rat pancreas. The enhancing effect of GABA is partially mediated by inhibition of islet somatostatin release.

gamma-aminobutyric acid receptor; cholecystokinin; secretin; gastrin-releasing peptide


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Am J Physiol Endocrinol Metab, April 1, 2007; 292(4): E1201 - E1206.
[Abstract] [Full Text] [PDF]


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