Soderlund D M, Adams P M, Bloomquist J R
Biochem Biophys Res Commun. 1987 Jul 31;146(2):692-8. doi: 10.1016/0006-291x(87)90584-5.
The effects of avermectin B1a (AVM) on the gamma-aminobutyric acid (GABA) receptor-chloride ionophore complex of mouse and rat brain were determined using assays of basal and GABA-stimulated 36Cl-uptake by brain vesicles. In the mouse, AVM acted solely as a potent non-competitive inhibitor of GABA-dependent chloride uptake. In the rat, inhibition of GABA-dependent chloride uptake was potent but incomplete, and AVM applied in the chloride uptake medium stimulated chloride uptake in the absence of GABA. The data provide evidence for qualitative differences between the GABA receptor complexes of mouse and rat brain in their responses to AVM.
通过检测脑囊泡对基础状态及γ-氨基丁酸（GABA）刺激的36Cl摄取，确定了阿维菌素B1a（AVM）对小鼠和大鼠脑γ-氨基丁酸（GABA）受体-氯离子载体复合物的影响。在小鼠中，AVM仅作为GABA依赖性氯离子摄取的强效非竞争性抑制剂。在大鼠中，对GABA依赖性氯离子摄取的抑制作用很强但不完全，并且在氯离子摄取培养基中应用AVM可在无GABA的情况下刺激氯离子摄取。这些数据为小鼠和大鼠脑GABA受体复合物对AVM反应的质性差异提供了证据。
