Williams M, Risley E A
Eur J Pharmacol. 1982 Feb 5;77(4):307-12. doi: 10.1016/0014-2999(82)90133-9.
The binding of [3H] beta-carboline-3-carboxylate ethyl ester ([3H] beta-CCE), a ligand for the benzodiazepine receptor in the mammalian CNS, to rat cortical membranes, is enhanced by avermectin B1a and its therapeutic formulation, Ivermectin. In contrast to the effects of the avermectins on [3H]diazepam binding, which involve changes in both receptor affinity and number, increases in beta-CCE binding, which are much less than those observed for the benzodiazepine ligand, involve only alterations in receptor number. This Bmax increase is bicuculline insensitive whereas Ivermectin effects on benzodiazepine binding are partially antagonized by GABA antagonist. The data suggest a differential interaction by the avermectins on benzodiazepine and beta-CCE binding sites in rat cortical membranes and indicate that these macrolide anthelmintics may be a useful tool for characterizing benzodiazepine/anxiolytic receptor subtypes.
[3H]β-咔啉-3-羧酸乙酯（[3H]β-CCE）是哺乳动物中枢神经系统中苯二氮䓬受体的一种配体，它与大鼠皮层膜的结合会被阿维菌素B1a及其治疗制剂伊维菌素增强。与阿维菌素对[3H]地西泮结合的影响不同，后者涉及受体亲和力和数量的变化，β-CCE结合的增加（远低于苯二氮䓬配体所观察到的增加）仅涉及受体数量的改变。这种Bmax的增加对荷包牡丹碱不敏感，而伊维菌素对苯二氮䓬结合的影响会被GABA拮抗剂部分拮抗。数据表明阿维菌素对大鼠皮层膜中苯二氮䓬和β-CCE结合位点存在差异相互作用，并表明这些大环内酯类驱虫药可能是表征苯二氮䓬/抗焦虑受体亚型的有用工具。
