Graham D, Pfeiffer F, Betz H
Neurosci Lett. 1982 Apr 16;29(2):173-6. doi: 10.1016/0304-3940(82)90349-4.
The anthelmintic drug, avermectin B1a, has been reported to interfere with gamma-aminobutyric acid-mediated chloride conductance. Also, enhancement of diazepam binding to mammalian brain membranes by avermectin B1a has led to the suggestion that avermectin B1a interacts with the 'benzodiazepine receptor-gamma-aminobutyric acid receptor-chloride ionophore' complex. Here we report an interaction of avermectin B1a with the glycine receptor. The binding of the glycine receptor antagonist, strychnine, to both membranes and solubilized receptor from rat spinal cord, was inhibited by avermectin B1a with Ki values of 1.3 microM and 3.6 microM, and Hill coefficients of 0.46 and 0.62, respectively.
据报道，驱虫药阿维菌素B1a会干扰γ-氨基丁酸介导的氯离子传导。此外，阿维菌素B1a增强了地西泮与哺乳动物脑膜的结合，这表明阿维菌素B1a与“苯二氮䓬受体-γ-氨基丁酸受体-氯离子载体”复合物相互作用。在此，我们报告阿维菌素B1a与甘氨酸受体的相互作用。阿维菌素B1a抑制了甘氨酸受体拮抗剂士的宁与大鼠脊髓膜及可溶性受体的结合，其抑制常数（Ki值）分别为1.3微摩尔/升和3.6微摩尔/升，希尔系数分别为0.46和0.62。
