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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Selectivity of McN-A-343 in stimulating phosphoinositide hydrolysis mediated by M1 muscarinic receptors.

The potency and efficacy of McN-A-343 (McN) in stimulating phosphoinositide (PI) hydrolysis were investigated in Chinese hamster ovary cells transfected with the m1 and m3 muscarinic receptor genes, in comparison with carbamylcholine (CBC). In m1 cells, CBC and McN increased PI hydrolysis by 17- and 9-fold over basal, respectively, with corresponding EC50 values of 4.2 and 4.3 microM. Whereas the maximal stimulatory response to CBC was slightly less in m3 cells (11-fold over basal), McN elicited only up to a 2-fold increase in PI hydrolysis in these cells. Competition binding data with N-[3H]methylscopolamine showed that McN had a higher affinity in m1 than in m3 cells, whereas CBC did not differentiate well between the two receptor subtypes. The partial agonistic activity of McN was demonstrated by its ability to suppress the stimulation by CBC to its own maximal response in both cell lines in a dose-dependent manner and by its low efficacy and the absence of receptor spareness. The PI response to the full agonist CBC in m3 cells was associated with a larger receptor reserve than in m1 cells. Thus, differences in receptor spareness cannot account for the apparent selectivity of McN in activating m1 muscarinic receptors. Differences in the sensitivity of m1 and m3 cells to McN were not due to differences in receptor concentration, despite the fact that the receptor density in m1 cells was 2-fold higher than in m3 cells. Our results suggest an actual selectivity (but not necessarily specificity) of the effects of McN in increasing Pl hydrolysis mediated by M1 receptors.[1]


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