Braswell L M, Miller K W, Sauter J F
Br J Pharmacol. 1984 Sep;83(1):305-11. doi: 10.1111/j.1476-5381.1984.tb10147.x.
Octanol increases the binding of [3H]-acetylcholine to the desensitized state of the nicotinic receptor in postsynaptic membranes prepared from Torpedo californica. This increase in binding results from an increase in the affinity of [3H]-acetylcholine for its receptor without any change in the number of sites or the shape of the acetylcholine binding curve. High pressures of helium (300 atm) decrease [3H]-acetylcholine binding by a mechanism that changes only the affinity of acetylcholine binding. Helium pressure reverses the effect of octanol on the affinity of [3H]-acetylcholine for its receptor. This pressure reversal of the action of octanol at a postsynaptic membrane is consistent either with pressure counteracting an octanol-induced membrane expansion or with independent mechanisms for the actions of octanol and pressure. The data do not conform with a mechanism in which pressure displaces octanol from a binding site on the receptor protein.
辛醇可增加[³H]-乙酰胆碱与从加州电鳐制备的突触后膜中处于脱敏状态的烟碱型受体的结合。这种结合增加是由于[³H]-乙酰胆碱对其受体的亲和力增加，而位点数量或乙酰胆碱结合曲线的形状没有任何变化。高压氦气（300个大气压）通过仅改变乙酰胆碱结合亲和力的机制降低[³H]-乙酰胆碱的结合。氦气压力可逆转辛醇对[³H]-乙酰胆碱与其受体亲和力的影响。辛醇在突触后膜作用的这种压力逆转，要么与压力抵消辛醇诱导的膜扩张一致，要么与辛醇和压力作用的独立机制一致。这些数据不符合压力将辛醇从受体蛋白上的结合位点置换的机制。
