British Journal of Pharmacology · 1981 · 105 citations · 4 references
Life SciencesBiochemistryPharmacologyCell SignalingElectrophysiologySignal TransductionCholinergic PharmacologyIon Channel ConductanceIon Channel PharmacologyIon Channel PhysiologyIon ChannelsMembrane ExcitabilityAcetylcholine Receptor PharmacologyChannel Conductance RegulationChannelsIon Equilibrium PotentialMuscarinic Acetylcholine Receptor SignalingNicotinic Acetylcholine Receptor AgonismNicotinic Receptor PharmacologyPurinergic Receptor Signaling
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.
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