Abstract
1 The sensitivity of the nicotinic acetylcholine (ACh)-receptor, measured as the amplitude of ACh-current induced by iontophoretic application of ACh to the frog skeletal muscle endplate, was increased by the action of adenosine triphosphate (ATP) 2 This potentiation was not due to the effect of ATP on ACh-esterase, since the increase of the sensitivity could also be demonstrated by use of carbachol (CCh) 3 Kinetic analysis of the effect of ATP on the dose-response curve of CCh-current suggests that ATP increases the ACh-sensitivity by acting on the allosteric site of receptor-ionic channel complex without changing the affinity of ACh for its recognition site 4 The equilibrium potential and the life-time of the endplate current (e.p.c.) are not altered by the presence of ATP 5 These results suggest that ATP increases the ACh-sensitivity by increasing either the conductance of unit channels or the total number of available channels.