Pressure reversal of the action of octanol on postsynaptic membranes from Torpedo

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Abstract
1 Octanol increases the binding of [3H]-acetylcholine to the desensitized state of the nicotinic receptor in postsynaptic membranes prepared from Torpedo californica. 2 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. 3 High pressures of helium (300 atm) decrease [3H]-acetylcholine binding by a mechanism that changes only the affinity of acetylcholine binding. 4 Helium pressure reverses the effect of octanol on the affinity of [3H]-acetylcholine for its receptor. 5 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. 6 The data do not conform with a mechanism in which pressure displaces octanol from a binding site on the receptor protein.