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1 e central command influence) using Norcuron (curare).
2 ta (deltaTrp-57) subunits that interact with curare.
3 ine < nicotine < acetylcholine < carbachol < curare.
4 species differences in circuit responses to curare.
7 e-field areas, we have exposed the retina to curare, a nicotinic cholinergic antagonist, because spon
10 in seconds after contact and were blocked by curare and alpha-bungarotoxin, but not by TTX and Cd(2+)
13 he affinity of the 5HT3R for the antagonists curare and granisetron but has little effect on the affi
16 tagonist [alpha-bungarotoxin (alpha-BTX) and curare] binding, these results indicate that mAbs could
19 structural level, we studied binding of the curare derivatives d-tubocurarine (d-TC) and metocurine
22 The competitive antagonist d-tubocurarine (curare) has greater potency at mouse than at human 5-hyd
23 mutant receptor, H-K195E,V202I, had the same curare IC50 (133.8 +/- 6.38 nM) as that of the human rec
24 contribute to curare potency, given that the curare IC50's (concentration of drug that produces 50% i
27 eceptive fields of ganglion cells exposed to curare in hatchlings reared in normal light and dark cyc
28 aneous bursting was chronically blocked with curare in hatchlings, dark-induced expansion of receptiv
30 their sedative and hypotensive effect, their curare-like activity and structural framework have made
31 title compounds (19, 20ab, and 26) displayed curare-like effects of ultrashort duration in rhesus mon
32 at can be further enhanced by treatment with curare or alpha-BTX, suggesting that muscle paralysis ma
33 line receptor (nAChR)-blocking agents [e.g., curare or alpha-bungarotoxin (alpha-BTX)] prevents the d
36 ata suggest that loops C and F contribute to curare potency, given that the curare IC50's (concentrat
38 nstrate that blocking synaptic activity with curare reduces synaptic neuregulin expression in a dose-
40 This blocking mechanism was tested using curare to demonstrate the open channel nature of the blo