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Changes in acetylcholine receptor number in muscle from critically ill patients receiving muscle relaxants: an investigation of the molecular mechanism of prolonged paralysis.
TLDR
It is suggested that muscle relaxant-induced, denervation-like changes may at least be partially responsible for prolonged muscle paralysis after the long-term administration of muscle relaxants. Expand
METABOLITES OF PINACOLYL METHYLPHOSPHONOFLUORIDATE (SOMAN) AFTER ENZYMATIC HYDROLYSIS IN VITRO.
TLDR
Application of Analytical procedures for the characterization and quantitative estimation of phosphonic acids derived from Soman suggests that the principal, if not the only, metabolite of Soman incubated with rat plasma or liver tissue in vitro is pinacolyl methylphosphonic acid. Expand
Pressure reversal of the action of octanol on postsynaptic membranes from Torpedo
TLDR
This work has shown that the binding of [3H]‐acetylcholine to the desensitized state of the nicotinic receptor in postsynaptic membranes prepared from Torpedo californica is increased without any change in the number of sites or the shape of the acetyl choline binding curve. Expand
Actions of General Anesthetics on Acetylcholine Receptor-rich Membranes from Torpedo californica
TLDR
Systematic deviations in the Torpedo model suggest that: 1) lipid solubility is not a sufficient criterion for activity in Torpede; 2) lipidsolubility inTorpedo membranes deviates from that at the anesthetic site; or 3) more than one effect underlies the binding assay. Expand
On the question: is acetylcholinesterase an allosteric protein?
TLDR
Data are interpreted as evidence for an allosteric site mechanism capable of modulating activity at the catalytic surface of acetylcholinesterase, presumably through conformational changes in the enzyme. Expand
The perturbation of lipid bilayers by general anesthetics: a quantitative test of the disordered lipid hypothesis.
TLDR
The disordered lipid hypothesis is fairly successful at correlating the anesthetic potency data over a dose range of four orders of magnitude, but some problems remain how far these can be overcome by developing more realistic models within the framework of the hypothesis remains to be seen. Expand
Two pools of cholesterol in acetylcholine receptor-rich membranes from Torpedo.
TLDR
Cholesterol depletion was accompanied by a significant increase in bulk membrane fluidity as measured by electron spin resonance spectroscopy, but the equilibrium binding parameters of acetylcholine to its receptor were unaltered, suggesting strongly that there exist two pools of cholesterol in the AChR-rich Torpedo electroplax membrane: an easily depleted fraction that influences bulk fluidity, and a tightly-bound fraction perhaps surrounding the A ChR oligomer. Expand
THE EFFECT IN VITRO OF VOLATILE ANESTHETICS ON THE ACTIVITY OF CHOLINESTERASES 1
TLDR
The data suggest that the effect in vitro of volatile anesthetics on the catalytic activity of cholinesterases is a variable one and may be unrelated to anesthetic potency in vivo. Expand
Actions of pentobarbital enantiomers on nicotinic cholinergic receptors.
TLDR
These results are consistent with a model where low concentrations of pentobarbital act on the receptor by binding to allosteric sites that have higher affinity but lower stereoselectivity for the open channel conformation than for the resting conformation, whereas the highest concentrations ofpentobar bital act by nonspecific mechanisms mediated by general membrane perturbations. Expand
Barbiturates bind to an allosteric regulatory site on nicotinic acetylcholine receptor-rich membranes.
TLDR
The ability of barbiturates to bind to acetylcholine receptor-rich membranes purified from the electroplaques of Torpedo nobiliana was examined by centrifugation assay, establishing a mutual negative heterotropic interaction between barbiturate-binding sites and cholinergic binding sites on the nicotinic acetylCholine receptor from Torpede. Expand
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