Effects of γ-Aminobutyric Acid on Pancreatic Amylase Secretion Evoked by Sodium Oleate in Anesthetized Rats

Effects of γ-Aminobutyric Acid on Pancreatic Amylase Secretion Evoked by Sodium Oleate in Anesthetized Rats

<P> γ-Aminobutyric Acid (GABA) is contained in pancreatic islet β-cells although its physiological role in pancreatic exocrine function is completely unknown at the present time. Recently, we have reported that exogenous GABA enhances secretagogue-evoked exocrine secretion in the isolated, perfused rat pancreas. This study was aimed to investigate an effect of exogenous GABA on pancreatic exocrine secretion <I>in vivo</I> evoked by intestinal stimulation. Rats were anesthetized with urethane (1.4 g/kg) after 24-h fast with free access to water. GABA (10, 30 and 100μmol/kg/h), given intravenously, did not change spontaneous pancreatic amylase secretion but dose-dependently elevated the amylase secretion evoked by intraduodenal sodium oleate (0.05 <I>m</I>mol/h). GABA (30μmol/kg/h) also further increased the amylase secretion stimulated by CCK (30 <I>p</I>mol/kg/h) plus secretin (20 <I>p</I>mol/kg/h) but failed to modify the amylase secretion induced by secretin alone. GABA (10, 30 and 100μmol/kg/h) also dose-dependently elevated pancreatic amylase secretion evoked by CCK alone. Bicuculline (100μmol/kg/h), a GABA<SUB>A</SUB>-receptor antagonist, markedly reduced the GABA-enhanced pancreatic responses to sodium oleate, CCK plus secretin or CCK alone. The results indicate that GABA enhances the sodium oleate-evoked pancreatic amylase secretion via GABA<SUB>A</SUB>-receptors in anesthetized rats, which may account for elevating the action of CCK released by sodium oleate.