Catecholamines, insulin and ACTH increase quantal size at the frog neuromuscular junction.
The size of miniature end-plate potentials (m.e.p.p.s) and miniature end-plate currents (m.e.p.c.s) at frog neuromuscular junctions was increased by a factor of two or more following treatment with norepinephrine, epinephrine, a cAMP derivative, insulin or ACTH. The increase in size was reversible. These agents do not appear to alter the ACh noise spectrum or the reversal potential of the end-plate. They do not alter the binding of alpha-bungarotoxin. Therefore they may increase the quantity of acetylcholine (ACh) in a quantum.
D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000818:Animals; D001001:Anura; D002395:Catecholamines / Q000494:pharmacology*; D004837:Epinephrine / Q000494:pharmacology; D007328:Insulin / Q000494:pharmacology*; D008564:Membrane Potentials / Q000187:drug effects; D009045:Motor Endplate / Q000187:drug effects; D009469:Neuromuscular Junction / Q000187:drug effects*; D009638:Norepinephrine / Q000494:pharmacology; D011950:Receptors, Cholinergic / Q000187:drug effects
D002395:Catecholamines; D007328:Insulin; D011950:Receptors, Cholinergic; D000324:Adrenocorticotropic Hormone; D009638:Norepinephrine; D004837:Epinephrine