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• W185231612 abstract "Lophotoxin, a cyclic diterpenoid isolated from coral, irreversibly inactivates the nicotinic acetylcholine receptor on intact BC3H-1 cells. Inactivation can be prevented by simultaneous incubation of lophotoxin with nicotinic agonists and competitive antagonists but not by noncompetitive antagonists such as dibucaine. Analysis of lophotoxin inhibition of carbamylcholine-elicited 22Na+ permeability, KG/KGmax, in relation to the number of sites blocked, y, reveals a function showing greater curvature than the parabolic function kG/kGmax = (1 - y)2 found for cobra alpha-toxin inhibition of 22Na+ permeability. This relationship is consistent with lophotoxin not binding randomly to the two primary agonist-antagonist sites but rather exhibiting a preference for one of the two sites. Binding of lophotoxin to a single site per receptor oligomer is sufficient to render the receptor nonfunctional. A comparison of the concentration dependencies for occupation by competitive antagonists reveals a shift to lower antagonist concentrations and an increase in Hill coefficient to approach unity after partial occupation by lophotoxin. Competitive antagonists are known to bind to two sites of unequal affinity on the receptor, and the preferential site of lophotoxin inactivation is the site of lower affinity for the competitive antagonists. In the case of agonists fractional inactivation of sites by lophotoxin results in a loss of the positive cooperativity and a shift of the concentration dependence for carbamylcholine binding to higher agonist concentrations. Similar behavior is observed for cobra alpha-toxin inactivation, but a comparison of concentration dependencies for agonist binding following partial occupation by lophotoxin and cobra alpha-toxin reveals that lophotoxin blockade yields residual sites with a lower affinity and Hill coefficients for agonists closer to unity. These shifts in agonist and antagonist binding profiles are also in accord with preferential inactivation of one of the two agonist sites by lophotoxin. The findings indicate that the site of lower affinity for antagonists may possess the higher affinity for agonists." @default.
• W185231612 created "2016-06-24" @default.
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• W185231612 date "1984-03-01" @default.
• W185231612 modified "2023-10-13" @default.
• W185231612 title "Lophotoxin irreversibly inactivates the nicotinic acetylcholine receptor by preferential association at one of the two primary agonist sites." @default.
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• W185231612 doi "https://doi.org/10.1016/s0021-9258(17)43160-7" @default.
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