Meyer M R, Gainer M W, Nathanson N M
Mol Pharmacol. 1982 Mar;21(2):280-6.
Prolonged treatment of chick embryos in vivo with the muscarinic agonists oxotremorine or carbachol leads to dose- and time-dependent decreases in the number of brain muscarinic acetylcholine receptors (mAChR) as measured by the specific binding of the potent muscarinic ligand L-[3H]quinuclidinyl benzilate to brain membranes. Maximal doses of agonists reduced the number of mAChR as much as 44%. Maximal loss of mAChR occurs 4 hr after treatment, but can be prevented or totally reversed within 24 hr by blockade of agonist-receptor interactions with muscarinic antagonists. After sustained in vivo oxotremorine treatment, brain mAChR show a decreased apparent affinity for agonists owing to a decrease in the affinities of both the high- and low-affinity agonist binding sites.
用毒蕈碱激动剂氧化震颤素或卡巴胆碱对鸡胚进行体内长时间处理，会导致脑毒蕈碱型乙酰胆碱受体（mAChR）数量呈剂量和时间依赖性减少，这是通过强效毒蕈碱配体L-[3H]喹核醇基苯甲酸酯与脑膜的特异性结合来测量的。激动剂的最大剂量可使mAChR数量减少多达44%。mAChR的最大损失在处理后4小时出现，但通过用毒蕈碱拮抗剂阻断激动剂-受体相互作用，可在24小时内预防或完全逆转。在持续进行体内氧化震颤素处理后，由于高亲和力和低亲和力激动剂结合位点的亲和力降低，脑mAChR对激动剂的表观亲和力下降。
