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在豚鼠腹腔神经节细胞，γ－氨基丁酸（ＧＡＢＡ）可诱发“去极化－超极化”的双相反应，去极化伴膜电阻减小，超极化伴膜电阻增大，这种反应在低钙高镁液中仍然存在。蝇蕈醇可模拟ＧＡＢＡ双相反应，但在诱发相同强度的去极化反应时，蝇蕈醇产生的超极化弱于ＧＡＢＡ。荷包牡丹碱（１００μｍｏｌ／Ｌ）和印防已毒素（１００—３００μｍｏｌ／Ｌ）能可逆地抑制ＧＡＢＡ诱发的双相反应。Ｂａｃｌｏｆｅｎ对神经节细胞的膜电位无明显影响。结果提示，ＧＡＢＡ双相反应的去极化相由ＧＡＢＡＡ／Ｃｌ－通道受体复合物介导，而超极化相很可能由不同于经典的ＧＡＢＡＡ受体，但其药理学行为又由与之十分相近的另一种ＧＡＢＡ受体介导。
In guinea pig celiac ganglion cells, γ-aminobutyric acid (GABA) induces a biphasic “depolarization-hyperpolarization” bipolar reaction with decreased membrane resistance and hyperpolarization with increased membrane resistance, which The reaction is still present in low calcium and magnesium liquids. Muscimol can mimic the GABA biphasic response, but muscimol produces less hyperpolarization than GABA upon inducing the same intensity of depolarization. Bicupidine (100μmol / L) and printed toxin (100-300μmol / L) reversibly inhibited the GABA-induced biphasic response. Baclofen had no significant effect on the membrane potential of ganglion cells. The results suggest that the depolarizing phase of the GABA biphasic response is mediated by the GABAA / Cl-channel receptor complex, whereas the hyperpolarized phase is likely to be different from the classical GABAA receptor, but its pharmacological behavior by the Very similar to another GABA receptor-mediated.