Court J A, Piggott M A, Perry E K
MRC Neurochemical Pathology Unit, Newcastle General Hospital, Newcastle upon Tyne U.K.
Brain Res. 1990 Aug 6;524(2):319-21. doi: 10.1016/0006-8993(90)90708-j.
Nicotine (10 and 100 microM) inhibited [3H]MK-801 binding to rat cerebral cortical membranes and this effect was not blocked by dihydro-beta-erythroidine, (+)-tubocurarine or mecamylamine. Cytisine, muscarine mecamylamine and (+)-tubocurarine also inhibited [3H]MK-801 binding. Neither raising the MK-801 concentration, nor the addition of n-methyl-D-aspartate (NMDA) receptor agonists altered the effects of nicotine. Hence this response is not mediated via high-affinity nicotinic receptor stimulation, competition for MK-801 binding sites or require NMDA receptor activation.
尼古丁（10和100微摩尔）抑制[3H]MK-801与大鼠大脑皮质膜的结合，且二氢β-刺桐啶、（+）-筒箭毒碱或美加明不能阻断这种作用。金雀花碱、毒蕈碱、美加明和（+）-筒箭毒碱也抑制[3H]MK-801的结合。提高MK-801浓度或添加N-甲基-D-天冬氨酸（NMDA）受体激动剂均未改变尼古丁的作用。因此，这种反应不是通过高亲和力烟碱受体刺激、对MK-801结合位点的竞争介导的，也不需要NMDA受体激活。
