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1  and two antagonists (alpha-bungarotoxin and d-tubocurarine).
2 he presence of agonist (5-HT) or antagonist (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.
15             Cibacron blue (1-100 microM) and d-tubocurarine (0.1-1 mM) produced rapid (10 sec to 5 mi
16 s, dihydro-beta-erythroidine (10 microM) and d-tubocurarine (10 microM).
17  Myotube patch responses were antagonized by d-tubocurarine (3 microM).
18 ne was increased by carbamylcholine (90%) or d-tubocurarine (50%), but it was inhibited by isoflurane
19                                              d-Tubocurarine, a conformationally restricted 5-HT3 liga
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
22                                 Furthermore, d-tubocurarine alone blocked the development of both imm
23 ompetitive and non-competitive AChR blockers d-tubocurarine and alpha-bungarotoxin, respectively.
24 sence of the acetylcholine receptor blockers d-tubocurarine and alpha-bungarotoxin.
25 hibition with the site-selective antagonists d-tubocurarine and alpha-conotoxin MI.
26  carbachol, and the cholinergic antagonists, D-tubocurarine and atropine.
27 ng can be enhanced by monovalent cations and d-tubocurarine and may be subject to negative allosteric
28  yielding KI values of 58 and 105 microM for d-tubocurarine and nicotine, respectively.
29                               The binding of d-tubocurarine and several of its analogs to the mouse n
30                               The actions of d-tubocurarine and sodium were not additive.
31 eceptor antagonist), promethazine, atropine, d-tubocurarine and suramin had no obvious effects on osc
32                                Mecamylamine, d-tubocurarine, and hexamethonium blocked the function b
33 onists, including dihydro-beta-erythroidine, d-tubocurarine, and methyllycaconitine, also elicited si
34 itive antagonists of this receptor and, like d-tubocurarine, bind to the alphagamma site with much hi
35 ha subunit correlated with the high-affinity d-tubocurarine binding site, along with a lack of inhibi
36 pha subunit correlated with the low-affinity d-tubocurarine binding site, suggests that the 383C epit
37 ha subunit associated with the high-affinity d-tubocurarine binding site.
38       Further, the general nAChR antagonist, d-tubocurarine, blocked all but two of the observed chan
39 the bis(benzylisoquinoline) alkaloid family, d-(+)-tubocurarine chloride (DTC), has been evaluated as
40 ors in the periphery or cultured cell lines, D-tubocurarine chloride appears to be non-specific in bl
41                      A nicotinic antagonist, d-tubocurarine chloride, completely and reversibly block
42                   The competitive antagonist d-tubocurarine (curare) has greater potency at mouse tha
43 are inhibited by nanomolar concentrations of d-tubocurarine (curare) in a competitive fashion.
44      Here we delineate bound orientations of d-tubocurarine (d-TC) and its methylated derivative meto
45 we studied binding of the curare derivatives d-tubocurarine (d-TC) and metocurine to AChBP using comp
46  effects were depressed (not obliterated) by D-tubocurarine (D-TC), hexamethonium (C6) and atropine.A
47 nding of the site-selective ligands dimethyl-d-tubocurarine (DMT) and alpha-conotoxin M1 (CTX) confir
48 ities for the curariform antagonist dimethyl d-tubocurarine (DMT).
49 ptor affinity for the competitive antagonist d-tubocurarine (dTC) 5-35-fold.
50                                              d-Tubocurarine (dTC) evoked flickering activity of KAp c
51 arent affinity of the competitive antagonist d-tubocurarine (dTC) for the receptor.
52 inic acetylcholine receptor (nAChR) with [3H]d-tubocurarine (dTC) has identified a residue within the
53                                              d-Tubocurarine (dTC) is a potent competitive antagonist
54 y treated chicken embryos in ovo with either d-tubocurarine (dTC) or muscimol during the naturally oc
55 5 ns each are run with no ligand, antagonist d-tubocurarine (dTC), agonist acetylcholine (ACh), and a
56 amine binding of the competitive antagonist, d-tubocurarine (dTC), to the muscle-type nicotinic acety
57 ion by the reversible competitive antagonist d-tubocurarine (dTC).
58 letely blocked by a nonselective antagonist, d-tubocurarine, for nAChRs, but not by a selective antag
59 his alpha3/beta4 receptor was mecamylamine > d-tubocurarine > dihydro-beta-erythroidine > hexamethoni
60 with bicuculline or nicotinic receptors with d-tubocurarine had no effect, although exposure to nicot
61 CNS), we show that treatment with 100 microm d-tubocurarine has no effect on in-turbulence regulation
62 hydro-beta-erythroidine, methyllycaconitine, d-tubocurarine, hexamethonium, decamethonium, and mecamy
63  the concentration of ACh (IC50, ACh) and of d-tubocurarine (IC50,dTC) causing half-maximal retardati
64 placed by the specific nAChRalpha1 inhibitor d-tubocurarine in a dose-dependent manner.
65 r affects on the P2X4 purinoceptor and, like d-tubocurarine, increased [35S]ATPgammaS binding.
66 ese effects by the general nAChR antagonist, d-tubocurarine, indicated that gene expression changes a
67 was only slightly blocked by the antagonists d-tubocurarine, mecamylamine, or dihydro-beta-erythroidi
68 nt with nicotine or carbamylcholine, but not d-tubocurarine, mecamylamine, or dihydro-beta-erythroidi
69 nged by the blockers dihydrostreptomycin and d-tubocurarine nor by treatment of the apical membrane w
70 ffects, which were blocked by the antagonist d-tubocurarine, on the bacterial replication and cytokin
71 alpha7 AChRs was partially blocked by either d-tubocurarine or mecamylamine.
72 oduced a biphasic competition curve, whereas d-tubocurarine potentiated binding at concentrations in
73 brane current that was entirely prevented by d-tubocurarine preincubation or nAChRalpha1 silencing.
74     The complex effects of cibacron blue and d-tubocurarine seemed to be due to an allosteric interac
75                       Application of curare (d-tubocurarine) selectively blocked the Si3 synapses in
76 ed at non-up-regulating concentrations, only d-tubocurarine significantly inhibited agonist-induced u
77  free energy changes for carbamylcholine and d-tubocurarine, suggesting independent contributions of
78 addition of the K+ channel blockers, apamin, d-tubocurarine, tetraethylammonium (TEA), or intracellul
79  determined independently in the presence of d-tubocurarine to be -14 mV; the calculated potential at
80 halogenation at various functional groups on d-tubocurarine was measured to both the high affinity (a
81      Verapamil, tetrahydroaminoacridine, and d-tubocurarine were also sensitive to that chimeric subs
82 he antagonists dihydro-beta-erythroidine and d-tubocurarine were more potent at HS receptors.
83 ha4beta2, chlorisondamine, mecamylamine, and d-tubocurarine were, respectively, 100-, 8-, and 5-fold
84 e extracellular domain was inhibited >90% by d-tubocurarine, whereas addition of either carbamylcholi
85 Conversely, chronic in ovo administration of d-tubocurarine, which causes an increase in motoneuron b