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Pressure reversal of the action of octanol on postsynaptic membranes from Torpedo
Author(s) -
Braswell L.M.,
Miller K.W.,
Sauter J.F.
Publication year - 1984
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1984.tb10147.x
Subject(s) - acetylcholine , acetylcholine receptor , postsynaptic potential , torpedo , chemistry , biophysics , nicotinic acetylcholine receptor , octanol , nicotinic agonist , membrane , receptor , stereochemistry , biochemistry , pharmacology , biology , partition coefficient , chromatography
1 Octanol increases the binding of [ 3 H]‐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 [ 3 H]‐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 [ 3 H]‐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 [ 3 H]‐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.