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Physiology, Biochemistry, and Pathology of Neuromuscular Transmission
Published in Marc H. De Baets, Hans J.G.H. Oosterhuis, Myasthenia Gravis, 2019
Vesamicol (AH 5183) interferes with neuromuscular transmission by inhibiting the vesicular uptake of ACh. As can be expected, its effect upon stimulation is not direct but visible only after a delay, because it takes time before a substantial part of the vesicular store is used up. Substances that interfere with the synthesis of ACh also affect the level of ACh in the tissue and the number of ACh molecules in a vesicle, but of course these are indirect effects.
Neurotransmission at Parasympathetic Nerve Endings
Published in Kenneth J. Broadley, Autonomic Pharmacology, 2017
Vesamicol (Figure 7.3) blocks transport of Ach into the vesicle and will therefore affect its availability for release by the nerve action potential. The pharmacology of vesamicol has already been described. It has inhibitory effects upon all cholinergic nerves and has no therapeutic uses.
In vitro models of neuromuscular junctions and their potential for novel drug discovery and development
Published in Expert Opinion on Drug Discovery, 2020
Olaia F Vila, Yihuai Qu, Gordana Vunjak-Novakovic
In terms of acetylcholine recycling, Charoensook and colleagues demonstrated the dose-dependent effect of various drugs that alter ACh recycling such as vesamicol, that inhibits the vesicular ACh transporter, acetylethylcholine mustard hydrochloride, that inhibits the choline acetyltransferase, and neostigmine an ACh esterase inhibitor, demonstrating the potential of their model to be used in pharmacological screening [68]. Steinbeck et al. also used an ACh esterase inhibitor, pyridostigmine, to improve NMJ function in their optogenetic MG model [59].