Agonist and inhibitory effects of pyridostigmine at the neuromuscular junction.
When all of the AChE at the endplate is irreversibly inhibited by phospholine iodide the ionophoretically induced ACh endplate currents are increased more than 10-fold in amplitude. The reversible AChE inhibitor pyridostigmine only increases the current to about half this value because its effects are obscured by receptor blocking. It was found that pyridostigmine can activate the receptor ion channels when released by ionophoresis at the endplate, thus suggesting that agonist-like desensitization could contribute to the blocking effects.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001001:Anura; D002800:Cholinesterase Inhibitors / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004456:Echothiophate Iodide / Q000494:pharmacology; D007478:Iontophoresis; D009045:Motor Endplate / Q000187:drug effects / Q000502:physiology; D009433:Neural Inhibition; D009469:Neuromuscular Junction / Q000187:drug effects* / Q000201:enzymology; D011729:Pyridostigmine Bromide / Q000494:pharmacology*
D002800:Cholinesterase Inhibitors; D004456:Echothiophate Iodide; D011729:Pyridostigmine Bromide; D000109:Acetylcholine