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• W2059315296 abstract "The alkaloids (-)physostigmine (Phy), galanthamine (Gal) and codeine (Cod), and several derivatives and homologous compounds, can act as noncompetitive agonists (NCA) of nicotinic acetylcholine receptors (nAChR) from Torpedo electrocytes, frog and mammalian muscle cells, clonal rat pheochromocytoma cells, cultured hippocampal neurons and several ectopic expression systems, by interacting with a binding site on the alpha-subunits of these nAChRs that is insensitive to the natural transmitter, acetylcholine (ACh), and ACh-competitive agonists and antagonists. Several endogenous ligands, including opioid-type compounds, can also act via this site, albeit at higher concentrations than is typical for the interaction with their cognate receptors. The NCA-evoked responses can be observed at the single-channel level but they do not summate to significant macroscopic currents, suggesting that the major role of NCAs is to act as co-agonists, thereby potentiating nAChR channel activation by the natural transmitter. In more general terms, noncompetitive agonists may constitute part of a chemical network, by which intercellular messengers, in addition to serving their cognate receptors, could modulate the sensitivity of other neuroreceptors to their archetypic ligands. Such a mode of action would make centrally acting NCAs interesting candidate drugs in the treatment of neuro-degenerative diseases." @default.
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• W2059315296 date "1995-01-01" @default.
• W2059315296 modified "2023-09-27" @default.
• W2059315296 title "Minireview: Noncompetitive Agonism at Nicotinic Acetylcholine Receptors; Functional Significance for CNS Signal Transduction" @default.
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• W2059315296 doi "https://doi.org/10.3109/10799899509045225" @default.
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