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- W2042895555 abstract "The interaction of 18-methoxycoronaridine (18-MC) with nicotinic acetylcholine receptors (AChRs) was compared with that for ibogaine and phencyclidine (PCP). The results established that 18-MC: (a) is more potent than ibogaine and PCP inhibiting (±)-epibatidine-induced AChR Ca2+ influx. The potency of 18-MC is increased after longer pre-incubation periods, which is in agreement with the enhancement of [3H]cytisine binding to resting but activatable Torpedo AChRs, (b) binds to a single site in the Torpedo AChR with high affinity and inhibits [3H]TCP binding to desensitized AChRs in a steric fashion, suggesting the existence of overlapping sites. This is supported by our docking results indicating that 18-MC interacts with a domain located between the serine (position 6′) and valine (position 13′) rings, and (c) inhibits [3H]TCP, [3H]ibogaine, and [3H]18-MC binding to desensitized AChRs with higher affinity compared to resting AChRs. This can be partially attributed to a slower dissociation rate from the desensitized AChR compared to that from the resting AChR. The enthalpic contribution is more important than the entropic contribution when 18-MC binds to the desensitized AChR compared to that for the resting AChR, and vice versa. Ibogaine analogs inhibit the AChR by interacting with a luminal domain that is shared with PCP, and by inducing desensitization." @default.
- W2042895555 created "2016-06-24" @default.
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- W2042895555 date "2010-06-01" @default.
- W2042895555 modified "2023-09-29" @default.
- W2042895555 title "Interaction of 18-methoxycoronaridine with nicotinic acetylcholine receptors in different conformational states" @default.
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- W2042895555 doi "https://doi.org/10.1016/j.bbamem.2010.03.013" @default.
- W2042895555 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3787694" @default.
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