El-Fakahany E E, Pfenning M, Richelson E
J Neurochem. 1984 Mar;42(3):863-9. doi: 10.1111/j.1471-4159.1984.tb02760.x.
Preincubation of murine neuroblastoma cells (clone N1E-115) with terbium chloride resulted in a significant potentiation of carbachol-mediated increase in cyclic GMP formation. This effect was accompanied by a shift of the peak response from 30 s to 120 s and a 6-fold decrease in carbachol concentration producing half-maximal responses, in addition to a significant increase in the Hill coefficient. Terbium ions also caused a significant decrease in the affinity and an increase in the maximum binding of [3H]quinuclidinyl benzilate to muscarinic receptors, the change in affinity being mainly due to a decrease in the association rate. Preincubation of cells with 1 mM carbachol for 4 h (the desensitized state of the muscarinic receptor) resulted in a decrease in the ability of terbium to alter [3H]quinuclidinyl benzilate binding. The effects of terbium reported here might be due to its affecting muscarinic receptor-effector coupling, which is considered to be lost upon receptor desensitization.
用氯化铽对小鼠神经母细胞瘤细胞(克隆N1E - 115)进行预孵育,可显著增强卡巴胆碱介导的环鸟苷酸生成增加。除了希尔系数显著增加外,这种效应还伴随着峰值反应从30秒移至120秒,以及产生半数最大反应的卡巴胆碱浓度降低6倍。铽离子还导致[3H]喹核醇基苯甲酸酯与毒蕈碱受体的亲和力显著降低,最大结合量增加,亲和力的变化主要是由于结合速率降低。用1 mM卡巴胆碱对细胞预孵育4小时(毒蕈碱受体的脱敏状态)会导致铽改变[3H]喹核醇基苯甲酸酯结合的能力下降。此处报道的铽的作用可能是由于其影响毒蕈碱受体 - 效应器偶联,而这种偶联被认为在受体脱敏时丧失。