Pressure reversal of the action of octanol on postsynaptic membranes from Torpedo.
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.
D020003:1-Octanol; D000109:Acetylcholine / Q000378:metabolism; D000777:Anesthetics / Q000494:pharmacology*; D000818:Animals; D005740:Gases; D006371:Helium; D066298:In Vitro Techniques; D000442:Octanols / Q000494:pharmacology*; D011312:Pressure; D011950:Receptors, Cholinergic / Q000187:drug effects*; D013570:Synaptic Membranes / Q000187:drug effects* / Q000378:metabolism; D014101:Torpedo
D000777:Anesthetics; D005740:Gases; D000442:Octanols; D011950:Receptors, Cholinergic; D006371:Helium; D000109:Acetylcholine; D020003:1-Octanol