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. 1984 Sep;83(1):305–311. doi: 10.1111/j.1476-5381.1984.tb10147.x

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

L M Braswell, K W Miller, J F Sauter
PMCID: PMC1987166  PMID: 6487895

Abstract

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.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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