Pressure reversal of the action of octanol on postsynaptic membranes from Torpedo
1984
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.
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