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1 -benzylidene anabaseine), and an antagonist (methyllycaconitine).
2 e nicotine acetylcholine receptor antagonist methyllycaconitine.
3 nt of the biphasic response was resistant to methyllycaconitine.
4 e blocked by the alpha7-selective antagonist methyllycaconitine.
5 ing (monophasic) current that was blocked by methyllycaconitine.
6 amine and dihydro-beta-erythroidine, but not methyllycaconitine.
7 tagonists alpha-bungarotoxin (alphaBgTx) and methyllycaconitine.
8         Another selective alpha7 antagonist, methyllycaconitine (0.05-5 microM), did not strongly inh
9 olinium (50 microM), adiphenine (50 microM), methyllycaconitine (1 microM) and alpha-bungarotoxin (1
10 and nicotine that were blocked reversibly by methyllycaconitine (1 nM) and irreversibly by alpha-bung
11  antagonists alpha-bungarotoxin (100 nM) and methyllycaconitine (10 nM) also inhibited the response t
12 urons tested, and this effect was blocked by methyllycaconitine (10 nM), suggesting a key role for al
13 e the norepinephrine effect was sensitive to methyllycaconitine (100 nM), it is concluded that nicoti
14 (3)H]NIC) binding (alpha4beta2 nAChR), [(3)H]methyllycaconitine ([(3)H]MLA) binding (alpha7 nAChR), a
15  LLTS, (2) LLTS with the alpha7nAchR blocker methyllycaconitine, (3) sham, and (4) olmesartan.
16 the neurons, which was completely blocked by methyllycaconitine, a specific antagonist of the alpha7
17                        The alpha7 antagonist methyllycaconitine abolished the effect of AR-R17779.
18 ine and lobeline, and nicotinic antagonists, methyllycaconitine, alpha-bungarotoxin, and alpha-cobrat
19 ation (25 microM), alpha7 nAChR antagonists (methyllycaconitine, alpha-conotoxin-ImI) and glutamate r
20 ects of Ani/Neo in CS mice were cancelled by methyllycaconitine (alpha7nAChR antagonist) and alpha7nA
21  Interestingly, the alpha 7 nAChR antagonist methyllycaconitine also significantly prevented reductio
22 lpha-lobeline, dihydro-beta-erythroidine and methyllycaconitine, also displayed similar rank ordering
23 hydro-beta-erythroidine, d-tubocurarine, and methyllycaconitine, also elicited significant increases
24 tion is sensitive to alpha7 nAChR antagonist methyllycaconitine, although the primed potentiation is
25 otine, because the BgtR-specific antagonists methyllycaconitine and alpha-Bgt block approximately 90%
26   Furthermore, the relaxation was blocked by methyllycaconitine and alpha-bungarotoxin (preferential
27 were blocked by the alpha7 nAChR antagonists methyllycaconitine and alpha-bungarotoxin and by a desen
28                 Evoked EPSPs were blocked by methyllycaconitine and alpha-bungarotoxin, antagonists t
29 ocked by the alpha7/alpha9-nAChR antagonists methyllycaconitine and alpha-bungarotoxin, as well as by
30 ic acetylcholine receptor (nAChR) antagonist methyllycaconitine and blocked by the non-alpha7 nAChR a
31                             The finding that methyllycaconitine and dihydro-beta-erythroidine (antago
32  The finding then that the nAChR antagonists methyllycaconitine and dihydro-beta-erythroidine facilit
33                                              Methyllycaconitine and strychnine, other blockers of nAC
34 rrents were blocked by the alpha7 antagonist methyllycaconitine and were abolished when Glu172 was mu
35                                              Methyllycaconitine, another antagonist of alpha7-contain
36 marker ligand and epibatidine, nicotine, and methyllycaconitine as the displacers.
37                                              Methyllycaconitine attenuated these effects, whereas olm
38                  Nanomolar concentrations of methyllycaconitine blocked the alpha Bgt-sensitive compo
39 lls was attenuated by alpha-bungarotoxin and methyllycaconitine but not by dihydro-beta-erythroidine.
40 on: (1) The specific alpha7 nAChR antagonist methyllycaconitine citrate (MLA) blocked the effect of n
41 oaddition of either the nicotinic antagonist methyllycaconitine citrate hydrate (MLA) (20 mM) or musc
42                    Chronic nicotine enhanced methyllycaconitine citrate hydrate-resistant, dihydro-be
43   The antagonists dihydro-beta-erythroidine, methyllycaconitine, d-tubocurarine, hexamethonium, decam
44                        The alpha7 antagonist methyllycaconitine did not affect choline signal amplitu
45 for blocking the analgesic response, whereas methyllycaconitine exhibited selectivity for the pressor
46 conformation upon binding of the antagonist, methyllycaconitine, further opens to accommodate the pep
47 similarly improved in the LLTS and LLTS plus methyllycaconitine groups but remained low in the other
48 uman neuroblastoma cells (rank order potency methyllycaconitine>1, 1-dimethyl-4-phenylpiperazinium>(-
49                    Pharmacologic inhibition (methyllycaconitine IC(50): 0.2-0.6 nM) or genetic deleti
50 hydro-beta-erythroidine (IC50 of 3-6 nM) and methyllycaconitine (IC50 of 40-135 nM) were not selectiv
51 icits induced by the alpha7 nAChR antagonist methyllycaconitine in rats, and in DBA/2 mice that exhib
52 nsitive to low concentrations (10-100 nM) of methyllycaconitine, indicating that typical alpha7-conta
53                                 In contrast, methyllycaconitine-insensitive nicotinic receptors can i
54  structure of the Delphinium norditerpenoid, methyllycaconitine (MLA) (1).
55 or the preferential alpha7 nAChR antagonist, methyllycaconitine (MLA) (13.50 and 27.00 microg per sid
56 th tetrodotoxin (TTX) (1 microM), but not by methyllycaconitine (MLA) (50 nM).
57 thermore, effects of alpha7 nAChR antagonist methyllycaconitine (MLA) and GABA were also tested.
58 bited by a selective alpha7-nAChR antagonist methyllycaconitine (MLA) and intracellular calcium chela
59 ptic currents by the alpha7-nAChR antagonist methyllycaconitine (MLA) and the agonist nicotine.
60 hR antagonists dihydro-beta-erythroidine and methyllycaconitine (MLA) and was absent in alpha7(-/-) m
61 ith either alpha-bungarotoxin (alpha-BGT) or methyllycaconitine (MLA) counteracted 60-75 % of the ACh
62                                              Methyllycaconitine (MLA) is known to be an antagonist of
63 to investigate interactions of 67 analogs of methyllycaconitine (MLA) on native alpha3beta4* nAChRs.
64     In contrast, the alpha7 antagonist alpha-methyllycaconitine (MLA) rescued ciliary neurons at 2.6
65   Local infusion of the nicotinic antagonist methyllycaconitine (MLA) to block alpha7 nicotinic recep
66 re blocked by the alpha7-specific antagonist methyllycaconitine (MLA) while increasing the percentage
67 alpha7 nicotinic receptor selective agonist, methyllycaconitine (MLA), an alpha7 receptor antagonist
68                                              Methyllycaconitine (MLA), an antagonist of alpha7 nAChR,
69 vented by alpha-bungaratoxin (alpha-Bgt) and methyllycaconitine (MLA), both selective alpha 7 antagon
70 t the alpha7-selective nicotinic antagonist, methyllycaconitine (MLA), protects against beta-amyloid-
71 pared to that for the competitive antagonist methyllycaconitine (MLA).
72 nds to the frequently used alpha7-antagonist methyllycaconitine (MLA).
73 ibited with the selective alpha7R antagonist methyllycaconitine (MLA).
74 t also the alpha7 nAChR-selective antagonist methyllycaconitine (MLA).
75 ked by the selective alpha7 nAChR antagonist methyllycaconitine (MLA).
76 subunit-specific antagonists: alpha-BgTx and methyllycaconitine (MLA).
77 scarine; ACh and alpha-bungarotoxin (Bgt) or methyllycaconitine (MLA); and glutamate and choline or g
78  alpha7-nAChR agonist choline and antagonist methyllycaconitine (MLA); while IIID receptor-mediated c
79 a7-nAChR (nicotinic ACh receptor)-selective [methyllycaconitine (MLA)] or beta2*-nAChR-selective [mec
80        The alpha7-selective nAChR antagonist methyllycaconitine (MLA; 50 nM) reduced the open probabi
81 urrents that, being sensitive to blockade by methyllycaconitine (MLA; 50 nM), were most likely subser
82 ing male rats, we found that PFC infusion of methyllycaconitine (MLA; a7nAChR antagonist) shifts vent
83 ihydro-beta-erythroidine, decamethonium, and methyllycaconitine; noncompetitive antagonism by mecamyl
84 he neuronal receptor, alpha-bungarotoxin and methyllycaconitine not only failed to block, but also ac
85 with either the alpha-7 nicotinic antagonist methyllycaconitine or the non-selective nicotinic antago
86 lpha-Ctx PIA (1 nm) but not by alpha7 (10 nm methyllycaconitine) or alpha4* (1 mum dihydro-beta-eryth
87                                              Methyllycaconitine released Src activity in intact KCs a
88                     In several interneurons, methyllycaconitine-sensitive spontaneous EPSCs also were
89   Null mice also lack rapidly desensitizing, methyllycaconitine-sensitive, nicotinic currents that ar
90 hroidine nor the selective alpha7 antagonist methyllycaconitine significantly blocked the nicotine-el
91 ponent was blocked by alpha-bungarotoxin and methyllycaconitine, suggesting that receptors contained
92 at cortex against [(3)H]-cytisine and [(3)H]-methyllycaconitine to measure their affinity for alpha4b
93                                              Methyllycaconitine was 9-fold more potent at inhibiting
94 ere tested with either alpha-bungarotoxin or methyllycaconitine, which are selective antagonists for