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1 ta2*-selective nAChR antagonist dihydro-beta-erythroidine.
2 nicotinic receptor antagonist di-hydro-beta-erythroidine.
3 of alpha-bungarotoxin but not di-hydro-beta-erythroidine.
4 ncy 17-fold higher than that of dihydro-beta-erythroidine.
5 d methyllycaconitine but not by dihydro-beta-erythroidine.
6 xin, but not by mecamylamine or dihydro-beta-erythroidine.
7 t by two nicotinic antagonists, dihydro-beta-erythroidine (10 microM) and d-tubocurarine (10 microM).
8 T were significantly blocked by dihydro-beta-erythroidine (10-20 nM), an antagonist of the alpha4beta
9 lly, mecamylamine (1 mg/kg) and dihydro-beta-erythroidine (2 mg/kg) - nicotinic antagonists - and atr
10 camylamine (100-500 microM) and dihydro-beta-erythroidine (250 microM) converted this mode of activit
11 ylamine but was not affected by dihydro-beta-erythroidine (a preferential alpha4-nAChR antagonist).
12 icotinic antagonists curare and dihydro-beta-erythroidine also up-regulated alpha3 beta2 AChRs, but o
13 Br-cytisine and the antagonists dihydro-beta-erythroidine and d-tubocurarine were more potent at HS r
14 ted by alpha7 nAChR antagonists dihydro-beta-erythroidine and methyllycaconitine (MLA) and was absent
15 or antagonists, alpha-lobeline, dihydro-beta-erythroidine and methyllycaconitine, also displayed simi
16 id residues that determine both dihydro-beta-erythroidine and neuronal bungarotoxin sensitivity are l
17 r antagonists hexamethonium and dihydro-beta-erythroidine and reduced by the P2X antagonist pyridoxal
18 cholinergic receptor antagonist dihydro-beta-erythroidine, and also when the rats were pretreated wit
19 ing that methyllycaconitine and dihydro-beta-erythroidine (antagonists of alpha7 and alpha4beta2 nACh
20 ected by alpha-conotoxin-MII or dihydro-beta-erythroidine, antagonists of alpha3/alpha6beta2* and bet
21 the alpha7 subunit, but not by dihydro-beta-erythroidine at concentrations known to antagonize alpha
22 -tubocurarine, mecamylamine, or dihydro-beta-erythroidine at concentrations that efficiently block al
27 line; competitive antagonism by dihydro-beta-erythroidine, decamethonium, and methyllycaconitine; non
29 ne receptor (nAChR) antagonists dihydro-beta-erythroidine (DH beta E, 100 microM) or mecamylamine (50
30 by mecamylamine (50 microM) or dihydro-beta-erythroidine (DH beta E; 1 microM) at concentrations kno
31 l alpha4beta2 nAChR antagonist, dihydro-beta-erythroidine (DHbetaE) (6.00 and 18.00 microg per side),
32 e nicotinic receptor antagonist dihydro-beta-erythroidine (DHbetaE) blocked the carbachol-induced enh
33 ifferent antagonists (10 microM dihydro-beta-erythroidine (DHbetaE) for nicotinic ACh receptors (nACh
34 agonists, mecamylamine (MEC) or dihydro-beta-erythroidine (DHbetaE) providing equivocal evidence for
35 ion of the nicotinic antagonist dihydro-beta-erythroidine (DHbetaE) to the buffer significantly atten
36 ed by nAChR antagonists Mec and Dihydro-beta-erythroidine (DHbetaE), and also by the DA D1 receptor a
37 gonists, mecamylamine (MEC) and dihydro-beta-erythroidine (DHbetaE), and by the dopamine (DA) (D1) an
38 agonists mecamylamine (MEC) and dihydro-beta-erythroidine (DHbetaE), but not by D-tubocurare (D-TC).
41 agonist RJR-2403 and antagonist dihydro-beta-erythroidine (DHbetaE); IID receptor-mediated current wa
42 tine-mediated LTP is blocked by dihydro-beta-erythroidine (DHbetaE, 1 microM), an antagonist having a
43 alpha-Conotoxin MII (20 nM), dihydro-beta-erythroidine (DHbetaE; 1 nM), and hexamethonium (300 mic
44 MLA, but instead was blocked by dihydro-beta-erythroidine (DHbetaE; 10 microM), a broad spectrum nACh
45 being sensitive to blockade by dihydro-beta-erythroidine (DHbetaE; 10 microM), were most likely subs
47 t of cells with (-)-nicotine or dihydro-beta-erythroidine differentially modulated the efficacy of ac
49 agonists methyllycaconitine and dihydro-beta-erythroidine facilitated glutamatergic transmission betw
51 beta2-nAChR subunit antagonist dihydro-beta-erythroidine had no effect on VTA- or PPN-evoked synapti
52 d on GABAergic interneurons via dihydro-beta-erythroidine hydrobromide (DHbetaE)-insensitive nicotini
53 tine citrate hydrate-resistant, dihydro-beta-erythroidine hydrobromide-sensitive nicotinic currents e
55 d by the classic ACh competitor dihydro-beta-erythroidine in a noncompetitive manner and that morante
56 ion of the nicotinic antagonist dihydro-beta-erythroidine in an alpha4beta2-selective concentration (
57 bungarotoxin, mecamylamine, and dihydro-beta-erythroidine, indicating involvement of alpha7-containin
58 -tubocurarine, mecamylamine, or dihydro-beta-erythroidine, induced a 500-600% increase in the number
60 classic competitive antagonist dihydro-beta-erythroidine inhibits morantel-evoked currents noncompet
61 y of the competitive antagonist dihydro-beta-erythroidine is >7000 times higher at alpha4/beta2 recep
64 elective alpha4beta2 antagonist dihydro-beta-erythroidine nor the selective alpha7 antagonist methyll
67 e alpha4beta2 nAChR antagonist, dihydro-beta-erythroidine, or the alpha7 nAChR antagonist, alpha-bung
68 ha4*-selective nAChR antagonist dihydro-beta-erythroidine produced opposite effects and blocked the n
69 ts of nicotine were mediated by dihydro beta-erythroidine-sensitive alpha3-containing nicotinic acety
70 4, causes a 9-fold decrease in dihydro-beta-erythroidine sensitivity and a 71-fold decrease in neuro
72 the non-alpha7 nAChR antagonist dihydro-beta-erythroidine, suggesting that both nicotine-mediated des
73 ta2-selective nAChR antagonist, dihydro-beta-erythroidine, suggests that loss of cholinergic efficacy
75 oncentrations of the antagonist dihydro-beta-erythroidine that was not observed for alpha7 nAChRs at
76 and was selectively blocked by dihydro-beta-erythroidine, thus explaining the residual motility of u
77 CtxMII-sensitive sites, whereas dihydro-beta-erythroidine was a 7-fold more potent inhibitor of the a
78 t when the nicotinic antagonist dihydro-beta-erythroidine was present along with acetylcholine (n = 7
79 , or the competitive antagonist dihydro-beta-erythroidine; we also tested mutant nAChRs that readily
81 etylcholine receptor antagonist dihydro-beta-erythroidine, with the 0.33 mg/kg dose of ondansetron bl
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