ライフサイエンスコーパス: dihydro-beta-erythroidine

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1 relatively beta2*-selective nAChR antagonist dihydro-beta-erythroidine.

2 m with a potency 17-fold higher than that of dihydro-beta-erythroidine.

3 ngarotoxin and methyllycaconitine but not by dihydro-beta-erythroidine.

4 pha-bungarotoxin, but not by mecamylamine or dihydro-beta-erythroidine.

5 1 microM), not by two nicotinic antagonists, dihydro-beta-erythroidine (10 microM) and d-tubocurarine

6 t to alpha-BGT were significantly blocked by dihydro-beta-erythroidine (10-20 nM), an antagonist of t

7 Systemically, mecamylamine (1 mg/kg) and dihydro-beta-erythroidine (2 mg/kg) - nicotinic antagoni

8 0 microM), mecamylamine (100-500 microM) and dihydro-beta-erythroidine (250 microM) converted this mo

9 ts) and mecamylamine but was not affected by dihydro-beta-erythroidine (a preferential alpha4-nAChR a

10 The nicotinic antagonists curare and dihydro-beta-erythroidine also up-regulated alpha3 beta2

11 isine, and 3-Br-cytisine and the antagonists dihydro-beta-erythroidine and d-tubocurarine were more p

12 TP was prevented by alpha7 nAChR antagonists dihydro-beta-erythroidine and methyllycaconitine (MLA) a

13 otinic receptor antagonists, alpha-lobeline, dihydro-beta-erythroidine and methyllycaconitine, also d

14 that amino acid residues that determine both dihydro-beta-erythroidine and neuronal bungarotoxin sens

15 tinic receptor antagonists hexamethonium and dihydro-beta-erythroidine and reduced by the P2X antagon

16 he nicotinic cholinergic receptor antagonist dihydro-beta-erythroidine, and also when the rats were p

17 The finding that methyllycaconitine and dihydro-beta-erythroidine (antagonists of alpha7 and alp

18 hat was unaffected by alpha-conotoxin-MII or dihydro-beta-erythroidine, antagonists of alpha3/alpha6b

19 Rs containing the alpha7 subunit, but not by dihydro-beta-erythroidine at concentrations known to ant

20 antagonists d-tubocurarine, mecamylamine, or dihydro-beta-erythroidine at concentrations that efficie

21 ction by a noncompetitive mechanism, whereas dihydro-beta-erythroidine blocked the function competiti

22 ese effects were blocked by mecamylamine and dihydro-beta-erythroidine, but not methyllycaconitine.

23 Antagonists, including dihydro-beta-erythroidine, d-tubocurarine, and methyllyc

24 suberyldicholine; competitive antagonism by dihydro-beta-erythroidine, decamethonium, and methyllyca

25 In contrast dihydro-beta-erythroidine (DH beta E) is a competitive a

26 c acetylcholine receptor (nAChR) antagonists dihydro-beta-erythroidine (DH beta E, 100 microM) or mec

27 nM), but not by mecamylamine (50 microM) or dihydro-beta-erythroidine (DH beta E; 1 microM) at conce

28 e preferential alpha4beta2 nAChR antagonist, dihydro-beta-erythroidine (DHbetaE) (6.00 and 18.00 micr

29 The nicotinic receptor antagonist dihydro-beta-erythroidine (DHbetaE) blocked the carbacho

30 Different antagonists (10 microM dihydro-beta-erythroidine (DHbetaE) for nicotinic ACh re

31 the nAChR antagonists, mecamylamine (MEC) or dihydro-beta-erythroidine (DHbetaE) providing equivocal

32 Further addition of the nicotinic antagonist dihydro-beta-erythroidine (DHbetaE) to the buffer signif

33 was attenuated by nAChR antagonists Mec and Dihydro-beta-erythroidine (DHbetaE), and also by the DA

34 wo nAChR antagonists, mecamylamine (MEC) and dihydro-beta-erythroidine (DHbetaE), and by the dopamine

35 the nAChR antagonists mecamylamine (MEC) and dihydro-beta-erythroidine (DHbetaE), but not by D-tubocu

36 bunit-containing nAChR-selective antagonist, dihydro-beta-erythroidine (DHbetaE).

37 4beta2-nAChR agonist RJR-2403 and antagonist dihydro-beta-erythroidine (DHbetaE); IID receptor-mediat

38 The nicotine-mediated LTP is blocked by dihydro-beta-erythroidine (DHbetaE, 1 microM), an antago

39 alpha-Conotoxin MII (20 nM), dihydro-beta-erythroidine (DHbetaE; 1 nM), and hexametho

40 naffected by MLA, but instead was blocked by dihydro-beta-erythroidine (DHbetaE; 10 microM), a broad

41 urrents that, being sensitive to blockade by dihydro-beta-erythroidine (DHbetaE; 10 microM), were mos

42 The antagonist dihydro-beta-erythroidine did not mimic the effects of A

43 Treatment of cells with (-)-nicotine or dihydro-beta-erythroidine differentially modulated the e

44 hereas the alpha4beta2-selective antagonist, dihydro-beta-erythroidine, does not.

45 the nAChR antagonists methyllycaconitine and dihydro-beta-erythroidine facilitated glutamatergic tran

46 receptor was mecamylamine > d-tubocurarine > dihydro-beta-erythroidine > hexamethonium.

47 The beta2-nAChR subunit antagonist dihydro-beta-erythroidine had no effect on VTA- or PPN-e

48 each other and on GABAergic interneurons via dihydro-beta-erythroidine hydrobromide (DHbetaE)-insensi

49 ethyllycaconitine citrate hydrate-resistant, dihydro-beta-erythroidine hydrobromide-sensitive nicotin

50 Whereas the antagonists dihydro-beta-erythroidine (IC50 of 3-6 nM) and methyllyc

51 were inhibited by the classic ACh competitor dihydro-beta-erythroidine in a noncompetitive manner and

52 ocal application of the nicotinic antagonist dihydro-beta-erythroidine in an alpha4beta2-selective co

53 ive to alpha-bungarotoxin, mecamylamine, and dihydro-beta-erythroidine, indicating involvement of alp

54 ne, but not d-tubocurarine, mecamylamine, or dihydro-beta-erythroidine, induced a 500-600% increase i

55 Nicotinic antagonists mecamylamine and dihydro-beta-erythroidine inhibited responses in both as

56 show that the classic competitive antagonist dihydro-beta-erythroidine inhibits morantel-evoked curre

57 The affinity of the competitive antagonist dihydro-beta-erythroidine is >7000 times higher at alpha

58 The antagonists dihydro-beta-erythroidine, methyllycaconitine, d-tubocur

59 (10 nm methyllycaconitine) or alpha4* (1 mum dihydro-beta-erythroidine)-nAChR-selective antagonists.

60 Neither the selective alpha4beta2 antagonist dihydro-beta-erythroidine nor the selective alpha7 antag

61 tors had little (mecamylamine) or no effect (dihydro-beta-erythroidine) on the ACh-induced currents.

62 onists, (+)-tubocurarine, hexamethonium, and dihydro-beta-erythroidine, only 2-15-fold.

63 ation with the alpha4beta2 nAChR antagonist, dihydro-beta-erythroidine, or the alpha7 nAChR antagonis

64 The alpha4*-selective nAChR antagonist dihydro-beta-erythroidine produced opposite effects and

65 optotic effects of nicotine were mediated by dihydro beta-erythroidine-sensitive alpha3-containing ni

66 ccurs in beta 4, causes a 9-fold decrease in dihydro-beta-erythroidine sensitivity and a 71-fold decr

67 ungarotoxin sensitivity and has no effect on dihydro-beta-erythroidine sensitivity.

68 d blocked by the non-alpha7 nAChR antagonist dihydro-beta-erythroidine, suggesting that both nicotine

69 Use of the beta2-selective nAChR antagonist, dihydro-beta-erythroidine, suggests that loss of choline

70 a 2 is 56-fold more sensitive to blockage by dihydro-beta-erythroidine than is alpha 3 beta 4.

71 vity to low concentrations of the antagonist dihydro-beta-erythroidine that was not observed for alph

72 tized rapidly and was selectively blocked by dihydro-beta-erythroidine, thus explaining the residual

73 ng the alpha-CtxMII-sensitive sites, whereas dihydro-beta-erythroidine was a 7-fold more potent inhib

74 ntirely absent when the nicotinic antagonist dihydro-beta-erythroidine was present along with acetylc

75 nist cytisine, or the competitive antagonist dihydro-beta-erythroidine; we also tested mutant nAChRs

76 The effect was blocked by dihydro-beta-erythroidine whereas alpha-bungarotoxin had

77 nicotinic acetylcholine receptor antagonist dihydro-beta-erythroidine, with the 0.33 mg/kg dose of o

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