论文部分内容阅读
本文报道用~(125)I—α—银环蛇毒素研究某些药物对N—胆碱受体(N—-AChR)部位的作用及对N—AChR代谢的影响。用~(125)I—α-银环蛇毒素直接结合作用的研究表明:100和500μM新斯的明、美斯的明、甲基新斯的明和吡啶斯的明等对N—AChR部应有不同程度的专一性阻断作用。而毒扁豆碱和催醒宁对N—AChR部位无直接作用。小剂量美斯的明可加快膜受体降解速率和减慢新生N—AChR掺入膜表面。苯巴比妥纳对N—AChR部应的结合作用很类似于筒简毒碱,主要是减少运功终板内的受体部位数,其受体结合指数(RBI)为0.67。对硫磷(E 605)不直接结合N—ACR部位。但增加运动终板外N—AChR部位的密度,其RBI为1.46。
This paper reports the effect of some drugs on N-acetylcholine receptor (N-AChR) and its effect on the metabolism of N-AChR using ~ (125) I -α-bungarotoxin. Studies with the direct binding of ~ (125) I -α-bungarotoxin showed that 100 and 500 μM neostigmine, metsudramine, methyl neostigmine and pyridostigmine, etc. on N-AChR should Have different degrees of specificity blocking effect. But physostigmine and reminder Ning N-AChR site has no direct effect. A small dose of metsmin can accelerate the rate of membrane receptor degradation and slow the incorporation of nascent N-AChR into the membrane surface. The binding effect of phenobarbital on N-AChR is similar to that of tubulin, mainly to reduce the number of receptor sites in the engineered plate, with a receptor binding index (RBI) of 0.67. Parathion (E 605) does not directly bind to the N-ACR site. However, increasing the density of N-AChR sites outside the motor end plate resulted in an RBI of 1.46.