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1 he presence of agonist (5-HT) or antagonist (d-tubocurarine).
2 and two antagonists (alpha-bungarotoxin and d-tubocurarine).
3 um>(-)nicotine>cytisine>carbamylch oli ne> /=d-tubocurarine).
4 isplaceable by the small molecule antagonist d-tubocurarine.
5 ntagonism by pancuronium, hexamethonium, and d-tubocurarine.
6 the presence of the nACh receptor antagonist d-tubocurarine.
7 taneous addition of the nicotinic antagonist d-tubocurarine.
8 blocked by coapplication of mecamylamine and d-tubocurarine.
9 , but surprisingly enhanced the affinity for d-tubocurarine.
10 lved in interacting with the 13'-position of d-tubocurarine.
11 ally by alpha-bungarotoxin and completely by D-tubocurarine.
12 sitivity to apamin and differential block by d-tubocurarine.
13 pamin-sensitive channels are also blocked by d-tubocurarine.
14 EPCs) in preparations partially blocked with d-tubocurarine.
18 ne was increased by carbamylcholine (90%) or d-tubocurarine (50%), but it was inhibited by isoflurane
20 times greater than observed previously with d-tubocurarine, a nonselective blocker of nicotinic rece
21 line with the higher ACh affinity and lower d-tubocurarine affinity of the alpha-delta binding site
25 ng can be enhanced by monovalent cations and d-tubocurarine and may be subject to negative allosteric
29 eceptor antagonist), promethazine, atropine, d-tubocurarine and suramin had no obvious effects on osc
31 onists, including dihydro-beta-erythroidine, d-tubocurarine, and methyllycaconitine, also elicited si
32 itive antagonists of this receptor and, like d-tubocurarine, bind to the alphagamma site with much hi
33 ha subunit correlated with the high-affinity d-tubocurarine binding site, along with a lack of inhibi
34 pha subunit correlated with the low-affinity d-tubocurarine binding site, suggests that the 383C epit
37 the bis(benzylisoquinoline) alkaloid family, d-(+)-tubocurarine chloride (DTC), has been evaluated as
38 ors in the periphery or cultured cell lines, D-tubocurarine chloride appears to be non-specific in bl
43 we studied binding of the curare derivatives d-tubocurarine (d-TC) and metocurine to AChBP using comp
44 effects were depressed (not obliterated) by D-tubocurarine (D-TC), hexamethonium (C6) and atropine.A
45 nding of the site-selective ligands dimethyl-d-tubocurarine (DMT) and alpha-conotoxin M1 (CTX) confir
50 inic acetylcholine receptor (nAChR) with [3H]d-tubocurarine (dTC) has identified a residue within the
52 y treated chicken embryos in ovo with either d-tubocurarine (dTC) or muscimol during the naturally oc
53 5 ns each are run with no ligand, antagonist d-tubocurarine (dTC), agonist acetylcholine (ACh), and a
54 amine binding of the competitive antagonist, d-tubocurarine (dTC), to the muscle-type nicotinic acety
56 letely blocked by a nonselective antagonist, d-tubocurarine, for nAChRs, but not by a selective antag
57 his alpha3/beta4 receptor was mecamylamine > d-tubocurarine > dihydro-beta-erythroidine > hexamethoni
58 with bicuculline or nicotinic receptors with d-tubocurarine had no effect, although exposure to nicot
59 CNS), we show that treatment with 100 microm d-tubocurarine has no effect on in-turbulence regulation
60 hydro-beta-erythroidine, methyllycaconitine, d-tubocurarine, hexamethonium, decamethonium, and mecamy
61 the concentration of ACh (IC50, ACh) and of d-tubocurarine (IC50,dTC) causing half-maximal retardati
64 ese effects by the general nAChR antagonist, d-tubocurarine, indicated that gene expression changes a
65 was only slightly blocked by the antagonists d-tubocurarine, mecamylamine, or dihydro-beta-erythroidi
66 nt with nicotine or carbamylcholine, but not d-tubocurarine, mecamylamine, or dihydro-beta-erythroidi
67 nged by the blockers dihydrostreptomycin and d-tubocurarine nor by treatment of the apical membrane w
68 ffects, which were blocked by the antagonist d-tubocurarine, on the bacterial replication and cytokin
70 oduced a biphasic competition curve, whereas d-tubocurarine potentiated binding at concentrations in
71 brane current that was entirely prevented by d-tubocurarine preincubation or nAChRalpha1 silencing.
72 The complex effects of cibacron blue and d-tubocurarine seemed to be due to an allosteric interac
74 ed at non-up-regulating concentrations, only d-tubocurarine significantly inhibited agonist-induced u
75 free energy changes for carbamylcholine and d-tubocurarine, suggesting independent contributions of
76 addition of the K+ channel blockers, apamin, d-tubocurarine, tetraethylammonium (TEA), or intracellul
77 determined independently in the presence of d-tubocurarine to be -14 mV; the calculated potential at
78 halogenation at various functional groups on d-tubocurarine was measured to both the high affinity (a
81 ha4beta2, chlorisondamine, mecamylamine, and d-tubocurarine were, respectively, 100-, 8-, and 5-fold
82 e extracellular domain was inhibited >90% by d-tubocurarine, whereas addition of either carbamylcholi
83 Conversely, chronic in ovo administration of d-tubocurarine, which causes an increase in motoneuron b
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