el-Fakahany E E, Ramkumar V, Lai W S
J Pharmacol Exp Ther. 1986 Aug;238(2):554-63.
The properties of the specific binding of the muscarinic receptor ligands [3H]quinuclidinyl benzilate and N-[3H]methylscopolamine in rat brain were compared. The specific binding of both ligands was affected equally by heat, phospholipase A2 and trypsin. N-[3H]methylscopolamine labeled only a fraction of the total muscarinic receptors recognized by [3H]quinuclidinyl benzilate in different brain areas and in the heart. Evidence is presented that N-[3H]methylscopolamine, in fact, binds to a subpopulation of [3H]quinuclidinyl benzilate binding sites. The distribution of the high-affinity binding sites of N-[3H]methylscopolamine did not show a different tissue dependence as compared to the total receptor population, and did not parallel the distribution of the pirenzepine-sensitive M1 receptor subtype. Similarly, the affinity of both [3H]quinuclidinyl benzilate and N-[3H]methylscopolamine varied from one tissue to another by a maximum of 2-fold. Although (-)-quinuclidinyl benzilate competed for the specific binding of [3H]quinuclidinyl benzilate in different tissues according to the law of mass-action, N-methylscopolamine showed an anomalous interaction with two binding sites. The low-affinity binding sites of N-methylscopolamine showed saturability of [3H]quinuclidinyl benzilate binding and stereoselectivity. When the binding characteristics of these N-methylscopolamine-inaccessible binding sites of [3H]quinuclidinyl benzilate in the brain were investigated further, it was found that N-methylscopolamine bound exclusively with a single low affinity, whereas pirenzepine still interacted with two receptor populations incorporated in these sites. It is concluded from several lines of evidence that the heterogeneity of binding of N-methylscopolamine to muscarinic receptors does not represent an interaction with the muscarinic M1 and M2 receptor subtypes defined by pirenzepine. Thus, the unique binding profile of pirenzepine to muscarinic receptors cannot be explained merely on the basis of its hydrophilic nature.
比较了毒蕈碱受体配体[3H]喹核醇基苯甲酸酯和N-[3H]甲基东莨菪碱在大鼠脑中特异性结合的特性。两种配体的特异性结合受加热、磷脂酶A2和胰蛋白酶的影响程度相同。在不同脑区和心脏中,N-[3H]甲基东莨菪碱仅标记了[3H]喹核醇基苯甲酸酯识别的总毒蕈碱受体的一部分。有证据表明,N-[3H]甲基东莨菪碱实际上与[3H]喹核醇基苯甲酸酯结合位点的一个亚群结合。与总受体群体相比,N-[3H]甲基东莨菪碱高亲和力结合位点的分布没有显示出不同的组织依赖性,也不与哌仑西平敏感的M1受体亚型的分布平行。同样,[3H]喹核醇基苯甲酸酯和N-[3H]甲基东莨菪碱的亲和力在不同组织之间的变化最大为2倍。尽管(-)-喹核醇基苯甲酸酯根据质量作用定律竞争不同组织中[3H]喹核醇基苯甲酸酯的特异性结合,但N-甲基东莨菪碱与两个结合位点表现出异常相互作用。N-甲基东莨菪碱的低亲和力结合位点显示出[3H]喹核醇基苯甲酸酯结合的饱和性和立体选择性。当进一步研究脑中这些N-甲基东莨菪碱无法接近的[3H]喹核醇基苯甲酸酯结合位点的结合特性时,发现N-甲基东莨菪碱仅以单一低亲和力结合,而哌仑西平仍与包含在这些位点中的两个受体群体相互作用。从多条证据得出结论,N-甲基东莨菪碱与毒蕈碱受体结合的异质性并不代表与哌仑西平定义的毒蕈碱M1和M2受体亚型的相互作用。因此,哌仑西平与毒蕈碱受体独特的结合特征不能仅仅基于其亲水性来解释。