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1 ly beta2*-selective nAChR antagonist dihydro-beta-erythroidine.
2 beta2 nicotinic receptor antagonist di-hydro-beta-erythroidine.
3 ation of alpha-bungarotoxin but not di-hydro-beta-erythroidine.
4 potency 17-fold higher than that of dihydro-beta-erythroidine.
5 in and methyllycaconitine but not by dihydro-beta-erythroidine.
6 arotoxin, but not by mecamylamine or dihydro-beta-erythroidine.
7 ), not by two nicotinic antagonists, dihydro-beta-erythroidine (10 microM) and d-tubocurarine (10 mic
8 ha-BGT were significantly blocked by dihydro-beta-erythroidine (10-20 nM), an antagonist of the alpha
9 emically, mecamylamine (1 mg/kg) and dihydro-beta-erythroidine (2 mg/kg) - nicotinic antagonists - an
10 ), mecamylamine (100-500 microM) and dihydro-beta-erythroidine (250 microM) converted this mode of ac
11 mecamylamine but was not affected by dihydro-beta-erythroidine (a preferential alpha4-nAChR antagonis
12 The nicotinic antagonists curare and dihydro-beta-erythroidine also up-regulated alpha3 beta2 AChRs,
13 nd 3-Br-cytisine and the antagonists dihydro-beta-erythroidine and d-tubocurarine were more potent at
14 revented by alpha7 nAChR antagonists dihydro-beta-erythroidine and methyllycaconitine (MLA) and was a
15 eceptor antagonists, alpha-lobeline, dihydro-beta-erythroidine and methyllycaconitine, also displayed
16 no acid residues that determine both dihydro-beta-erythroidine and neuronal bungarotoxin sensitivity
17 ceptor antagonists hexamethonium and dihydro-beta-erythroidine and reduced by the P2X antagonist pyri
18 inic cholinergic receptor antagonist dihydro-beta-erythroidine, and also when the rats were pretreate
19 finding that methyllycaconitine and dihydro-beta-erythroidine (antagonists of alpha7 and alpha4beta2
20 unaffected by alpha-conotoxin-MII or dihydro-beta-erythroidine, antagonists of alpha3/alpha6beta2* an
21 ining the alpha7 subunit, but not by dihydro-beta-erythroidine at concentrations known to antagonize
22 sts d-tubocurarine, mecamylamine, or dihydro-beta-erythroidine at concentrations that efficiently blo
24 a noncompetitive mechanism, whereas dihydro-beta-erythroidine blocked the function competitively.
27 dicholine; competitive antagonism by dihydro-beta-erythroidine, decamethonium, and methyllycaconitine
29 choline receptor (nAChR) antagonists dihydro-beta-erythroidine (DH beta E, 100 microM) or mecamylamin
30 t not by mecamylamine (50 microM) or dihydro-beta-erythroidine (DH beta E; 1 microM) at concentration
31 ential alpha4beta2 nAChR antagonist, dihydro-beta-erythroidine (DHbetaE) (6.00 and 18.00 microg per s
32 The nicotinic receptor antagonist dihydro-beta-erythroidine (DHbetaE) blocked the carbachol-induce
34 R antagonists, mecamylamine (MEC) or dihydro-beta-erythroidine (DHbetaE) providing equivocal evidence
35 addition of the nicotinic antagonist dihydro-beta-erythroidine (DHbetaE) to the buffer significantly
36 enuated by nAChR antagonists Mec and Dihydro-beta-erythroidine (DHbetaE), and also by the DA D1 recep
37 antagonists, mecamylamine (MEC) and dihydro-beta-erythroidine (DHbetaE), and by the dopamine (DA) (D
38 R antagonists mecamylamine (MEC) and dihydro-beta-erythroidine (DHbetaE), but not by D-tubocurare (D-
41 AChR agonist RJR-2403 and antagonist dihydro-beta-erythroidine (DHbetaE); IID receptor-mediated curre
42 nicotine-mediated LTP is blocked by dihydro-beta-erythroidine (DHbetaE, 1 microM), an antagonist hav
44 d by MLA, but instead was blocked by dihydro-beta-erythroidine (DHbetaE; 10 microM), a broad spectrum
45 that, being sensitive to blockade by dihydro-beta-erythroidine (DHbetaE; 10 microM), were most likely
47 atment of cells with (-)-nicotine or dihydro-beta-erythroidine differentially modulated the efficacy
49 R antagonists methyllycaconitine and dihydro-beta-erythroidine facilitated glutamatergic transmission
51 The beta2-nAChR subunit antagonist dihydro-beta-erythroidine had no effect on VTA- or PPN-evoked sy
52 er and on GABAergic interneurons via dihydro-beta-erythroidine hydrobromide (DHbetaE)-insensitive nic
53 aconitine citrate hydrate-resistant, dihydro-beta-erythroidine hydrobromide-sensitive nicotinic curre
55 ibited by the classic ACh competitor dihydro-beta-erythroidine in a noncompetitive manner and that mo
56 lication of the nicotinic antagonist dihydro-beta-erythroidine in an alpha4beta2-selective concentrat
57 lpha-bungarotoxin, mecamylamine, and dihydro-beta-erythroidine, indicating involvement of alpha7-cont
58 not d-tubocurarine, mecamylamine, or dihydro-beta-erythroidine, induced a 500-600% increase in the nu
59 cotinic antagonists mecamylamine and dihydro-beta-erythroidine inhibited responses in both assays.
60 t the classic competitive antagonist dihydro-beta-erythroidine inhibits morantel-evoked currents nonc
61 finity of the competitive antagonist dihydro-beta-erythroidine is >7000 times higher at alpha4/beta2
64 the selective alpha4beta2 antagonist dihydro-beta-erythroidine nor the selective alpha7 antagonist me
67 th the alpha4beta2 nAChR antagonist, dihydro-beta-erythroidine, or the alpha7 nAChR antagonist, alpha
68 e alpha4*-selective nAChR antagonist dihydro-beta-erythroidine produced opposite effects and blocked
69 effects of nicotine were mediated by dihydro beta-erythroidine-sensitive alpha3-containing nicotinic
70 beta 4, causes a 9-fold decrease in dihydro-beta-erythroidine sensitivity and a 71-fold decrease in
72 d by the non-alpha7 nAChR antagonist dihydro-beta-erythroidine, suggesting that both nicotine-mediate
73 he beta2-selective nAChR antagonist, dihydro-beta-erythroidine, suggests that loss of cholinergic eff
75 low concentrations of the antagonist dihydro-beta-erythroidine that was not observed for alpha7 nAChR
76 pidly and was selectively blocked by dihydro-beta-erythroidine, thus explaining the residual motility
77 lpha-CtxMII-sensitive sites, whereas dihydro-beta-erythroidine was a 7-fold more potent inhibitor of
78 absent when the nicotinic antagonist dihydro-beta-erythroidine was present along with acetylcholine (
79 isine, or the competitive antagonist dihydro-beta-erythroidine; we also tested mutant nAChRs that rea
81 ic acetylcholine receptor antagonist dihydro-beta-erythroidine, with the 0.33 mg/kg dose of ondansetr
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