ライフサイエンスコーパス: methyllycaconitine

1 -benzylidene anabaseine), and an antagonist (methyllycaconitine).

2 nt of the biphasic response was resistant to methyllycaconitine.

3 e blocked by the alpha7-selective antagonist methyllycaconitine.

4 ing (monophasic) current that was blocked by methyllycaconitine.

5 amine and dihydro-beta-erythroidine, but not methyllycaconitine.

6 tagonists alpha-bungarotoxin (alphaBgTx) and methyllycaconitine.

7 e nicotine acetylcholine receptor antagonist 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 the neurons, which was completely blocked by methyllycaconitine, a specific antagonist of the alpha7

16 The alpha7 antagonist methyllycaconitine abolished the effect of AR-R17779.

17 ine and lobeline, and nicotinic antagonists, methyllycaconitine, alpha-bungarotoxin, and alpha-cobrat

18 ation (25 microM), alpha7 nAChR antagonists (methyllycaconitine, alpha-conotoxin-ImI) and glutamate r

19 ects of Ani/Neo in CS mice were cancelled by methyllycaconitine (alpha7nAChR antagonist) and alpha7nA

20 Interestingly, the alpha 7 nAChR antagonist methyllycaconitine also significantly prevented reductio

21 lpha-lobeline, dihydro-beta-erythroidine and methyllycaconitine, also displayed similar rank ordering

22 hydro-beta-erythroidine, d-tubocurarine, and methyllycaconitine, also elicited significant increases

23 tion is sensitive to alpha7 nAChR antagonist methyllycaconitine, although the primed potentiation is

24 otine, because the BgtR-specific antagonists methyllycaconitine and alpha-Bgt block approximately 90%

25 Furthermore, the relaxation was blocked by methyllycaconitine and alpha-bungarotoxin (preferential

26 were blocked by the alpha7 nAChR antagonists methyllycaconitine and alpha-bungarotoxin and by a desen

27 Evoked EPSPs were blocked by methyllycaconitine and alpha-bungarotoxin, antagonists t

28 ocked by the alpha7/alpha9-nAChR antagonists methyllycaconitine and alpha-bungarotoxin, as well as by

29 ic acetylcholine receptor (nAChR) antagonist methyllycaconitine and blocked by the non-alpha7 nAChR a

30 The finding that methyllycaconitine and dihydro-beta-erythroidine (antago

31 The finding then that the nAChR antagonists methyllycaconitine and dihydro-beta-erythroidine facilit

32 Methyllycaconitine and strychnine, other blockers of nAC

33 rrents were blocked by the alpha7 antagonist methyllycaconitine and were abolished when Glu172 was mu

34 Methyllycaconitine, another antagonist of alpha7-contain

35 marker ligand and epibatidine, nicotine, and methyllycaconitine as the displacers.

36 Nanomolar concentrations of methyllycaconitine blocked the alpha Bgt-sensitive compo

37 lls was attenuated by alpha-bungarotoxin and methyllycaconitine but not by dihydro-beta-erythroidine.

38 on: (1) The specific alpha7 nAChR antagonist methyllycaconitine citrate (MLA) blocked the effect of n

39 oaddition of either the nicotinic antagonist methyllycaconitine citrate hydrate (MLA) (20 mM) or musc

40 Chronic nicotine enhanced methyllycaconitine citrate hydrate-resistant, dihydro-be

41 The antagonists dihydro-beta-erythroidine, methyllycaconitine, d-tubocurarine, hexamethonium, decam

42 The alpha7 antagonist methyllycaconitine did not affect choline signal amplitu

43 for blocking the analgesic response, whereas methyllycaconitine exhibited selectivity for the pressor

44 conformation upon binding of the antagonist, methyllycaconitine, further opens to accommodate the pep

45 uman neuroblastoma cells (rank order potency methyllycaconitine>1, 1-dimethyl-4-phenylpiperazinium>(-

46 Pharmacologic inhibition (methyllycaconitine IC(50): 0.2-0.6 nM) or genetic deleti

47 hydro-beta-erythroidine (IC50 of 3-6 nM) and methyllycaconitine (IC50 of 40-135 nM) were not selectiv

48 icits induced by the alpha7 nAChR antagonist methyllycaconitine in rats, and in DBA/2 mice that exhib

49 nsitive to low concentrations (10-100 nM) of methyllycaconitine, indicating that typical alpha7-conta

50 In contrast, methyllycaconitine-insensitive nicotinic receptors can i

51 structure of the Delphinium norditerpenoid, methyllycaconitine (MLA) (1).

52 or the preferential alpha7 nAChR antagonist, methyllycaconitine (MLA) (13.50 and 27.00 microg per sid

53 th tetrodotoxin (TTX) (1 microM), but not by methyllycaconitine (MLA) (50 nM).

54 bited by a selective alpha7-nAChR antagonist methyllycaconitine (MLA) and intracellular calcium chela

55 ptic currents by the alpha7-nAChR antagonist methyllycaconitine (MLA) and the agonist nicotine.

56 hR antagonists dihydro-beta-erythroidine and methyllycaconitine (MLA) and was absent in alpha7(-/-) m

57 ith either alpha-bungarotoxin (alpha-BGT) or methyllycaconitine (MLA) counteracted 60-75 % of the ACh

58 Methyllycaconitine (MLA) is known to be an antagonist of

59 to investigate interactions of 67 analogs of methyllycaconitine (MLA) on native alpha3beta4* nAChRs.

60 In contrast, the alpha7 antagonist alpha-methyllycaconitine (MLA) rescued ciliary neurons at 2.6

61 Local infusion of the nicotinic antagonist methyllycaconitine (MLA) to block alpha7 nicotinic recep

62 re blocked by the alpha7-specific antagonist methyllycaconitine (MLA) while increasing the percentage

63 alpha7 nicotinic receptor selective agonist, methyllycaconitine (MLA), an alpha7 receptor antagonist

64 Methyllycaconitine (MLA), an antagonist of alpha7 nAChR,

65 vented by alpha-bungaratoxin (alpha-Bgt) and methyllycaconitine (MLA), both selective alpha 7 antagon

66 t the alpha7-selective nicotinic antagonist, methyllycaconitine (MLA), protects against beta-amyloid-

67 pared to that for the competitive antagonist methyllycaconitine (MLA).

68 nds to the frequently used alpha7-antagonist methyllycaconitine (MLA).

69 ibited with the selective alpha7R antagonist methyllycaconitine (MLA).

70 ked by the selective alpha7 nAChR antagonist methyllycaconitine (MLA).

71 t also the alpha7 nAChR-selective antagonist methyllycaconitine (MLA).

72 subunit-specific antagonists: alpha-BgTx and methyllycaconitine (MLA).

73 scarine; ACh and alpha-bungarotoxin (Bgt) or methyllycaconitine (MLA); and glutamate and choline or g

74 alpha7-nAChR agonist choline and antagonist methyllycaconitine (MLA); while IIID receptor-mediated c

75 a7-nAChR (nicotinic ACh receptor)-selective [methyllycaconitine (MLA)] or beta2*-nAChR-selective [mec

76 The alpha7-selective nAChR antagonist methyllycaconitine (MLA; 50 nM) reduced the open probabi

77 urrents that, being sensitive to blockade by methyllycaconitine (MLA; 50 nM), were most likely subser

78 ihydro-beta-erythroidine, decamethonium, and methyllycaconitine; noncompetitive antagonism by mecamyl

79 he neuronal receptor, alpha-bungarotoxin and methyllycaconitine not only failed to block, but also ac

80 with either the alpha-7 nicotinic antagonist methyllycaconitine or the non-selective nicotinic antago

81 lpha-Ctx PIA (1 nm) but not by alpha7 (10 nm methyllycaconitine) or alpha4* (1 mum dihydro-beta-eryth

82 Methyllycaconitine released Src activity in intact KCs a

83 In several interneurons, methyllycaconitine-sensitive spontaneous EPSCs also were

84 Null mice also lack rapidly desensitizing, methyllycaconitine-sensitive, nicotinic currents that ar

85 hroidine nor the selective alpha7 antagonist methyllycaconitine significantly blocked the nicotine-el

86 ponent was blocked by alpha-bungarotoxin and methyllycaconitine, suggesting that receptors contained

87 Methyllycaconitine was 9-fold more potent at inhibiting

88 ere tested with either alpha-bungarotoxin or methyllycaconitine, which are selective antagonists for