To explore the effects and the mechanism of gamma-aminobutyric acid (GABA) on gastric acid secretion (GAS) of isolated mouse stomach with perfused lumen, 12 cm H2O column intragastric pressure-provided. Whole stomach preparations from mice were incubated in buffer at 37degreeC in vitro, and perfusate was measured for pH with a pHS-3 type pH meter. The results shown that GABA (1apprx10X10-7 mol/L) and baclofen (Bac) (0. 6apprx9.6X10-7 mol/L) significantly promoted GAS in a concentration-dependent manner, whereas cimetidine (Cim) (2apprx20X10-7 mol/L) potently inhibited GAS in the same manner. Picrotoxin (Pic) (3X10-7 mol/L) did not affect basal gastric acid secretion (BGAS) and the promotive effect of GABA on GAS. Phaclofen (Phac) (0.6X10-7 mol/L) completely inhibited the promotive effect of GABA on GAS. Cim did not completely eliminate the promotive effects of GABA and Bac on GAS in isolated mouse stomach. Above results suggest that in mouse, GABA may promote GAS in isolated stomach, possibly by affecting GABAB receptors on both cholinergic neurons and non-neuronal cells, such as parietal cells and some endocrine cells. GABA may stimulate parietal cells to secrete acid directly or indirectly.