ライフサイエンスコーパス: alpha-conotoxin MII

1 d with the alpha3beta2-preferring antagonist alpha-conotoxin MII.

2 y itself, but not in animals pretreated with alpha-conotoxin MII.

3 ontaining an alpha3/beta2 subunit interface (alpha-conotoxin MII 100-200 nm) resulted in reversible a

4 Conversely, the alpha3 beta2-specific alpha-conotoxin MII (100 nM) blocks 33% of striatal dopa

5 alpha-Conotoxin MII (20 nM), dihydro-beta-erythroidine (

6 Alpha-conotoxin MII, a peptide toxin isolated from Conus

7 Alpha-conotoxin MII, a selective ligand that discriminat

8 n of the alpha3beta2*/alpha6beta2* selective alpha-conotoxin MII (alpha-CTX MII) dose- and time-depen

9 w component was selectively blocked by 50 nM alpha-conotoxin MII (alpha-CTx-MII), which blocks mammal

10 In this study, we used a novel alpha-conotoxin MII (alpha-CtxMII) analog E11A to furthe

11 animals, alpha6beta2(*) nAChR blockade with alpha-conotoxin MII (alpha-CtxMII) decreased release wit

12 However, discovery that alpha-conotoxin MII (alpha-CtxMII) partially inhibits th

13 ially important in nicotine addiction, binds alpha-conotoxin MII (alpha-CtxMII) with high affinity an

14 re pharmacologically similar to native [125I]alpha-conotoxin MII (alpha-CtxMII)-binding and 3-(2(S)-a

15 The competitive antagonist alpha-conotoxin-MII (alpha-CTx-MII) is highly selective

16 pha-conotoxin PeIA bears high resemblance to alpha-conotoxins MII and GIC isolated from Conus magus a

17 , 5-iodo-A-85380, sazetidine-A, varenicline, alpha-conotoxin MII, and bPiDDB (N,N-dodecane-1,12-diyl-

18 nt of the giant fiber system is inhibited by alpha-conotoxins MII, AuIB, BuIA, EI, PeIA, and ImI.

19 bition constant of MII[H9A;L15A] for [(125)I]alpha-conotoxin MII binding to putative alpha6beta2(*) n

20 to identify a population of beta3-dependent alpha-conotoxin MII-binding nAChRs that modulate striata

21 alpha-Conotoxin MII (CtxMII), a peptide toxin from the v

22 For this purpose we used (125)I-alpha-conotoxin MII (CtxMII), a relatively new ligand th

23 ies for nicotine, cytisine, and A85380, that alpha-conotoxin MII discriminates between nAChR populati

24 Thus, structure-function analysis of alpha-conotoxin MII enabled the creation of novel select

25 Whereas alpha-conotoxin MII fully inhibits nicotine-evoked [3H]n

26 Intriguingly, alpha-conotoxin MII [H9A; L15A], blocked cocaine conditi

27 mbal injection of the selective alpha6beta2* alpha-conotoxin MII [H9A; L15A], blocked nicotine CPP.

28 alpha-conotoxin MII[H9A;L15A] also significantly reduced

29 t in VTA DAergic neurons that was blocked by alpha-conotoxin MII[H9A;L15A], a selective antagonist of

30 lasted several minutes and was sensitive to alpha-conotoxin MII[H9A;L15A].

31 The three-dimensional structure of alpha-conotoxin MII in aqueous solution has been determi

32 e (IR) binding of either labeled Epb or 125I-alpha-conotoxin MII increased to a much greater extent t

33 The recently discovered peptide alpha-conotoxin MII is a potent and selective inhibitor

34 alpha-Conotoxin MII, isolated from Conus magus, is a pot

35 Binding of [(125)I]alpha-conotoxin MII (largely to alpha6* nAChRs) did not

36 The alpha3/alpha6-selective antagonist alpha-conotoxin MII maximally inhibited 50% of binding i

37 which seemed to be due to a complete loss of alpha-conotoxin MII nAChRs and a partial loss of other n

38 ermore, two peptides structurally related to alpha-conotoxin MII, namely alpha-conotoxin MI (selectiv

39 However, neither alpha-conotoxin MII nor alpha-conotoxin GIC at concentra

40 (EC(50) = 1.2 microM) that was unaffected by alpha-conotoxin-MII or dihydro-beta-erythroidine, antago

41 ster (RTI-121, dopamine transporter), (125)I-alpha-conotoxin MII (putative alpha 6-containing sites i

42 ve nAChRs, and selected measures of striatal alpha-conotoxin MII-resistant nAChRs.

43 ed striatal dopamine release (both total and alpha-conotoxin MII-resistant release) increased with ag

44 tigated and did not discriminate between the alpha-conotoxin MII-sensitive and -insensitive populatio

45 lations in the caudate and putamen, and that alpha-conotoxin MII-sensitive nAChRs are selectively dec

46 binding and functional measures of striatal alpha-conotoxin MII-sensitive nAChRs, and selected measu

47 se in epibatidine binding was due to loss of alpha-conotoxin MII-sensitive nAChRs.

48 ta4 (alpha-conotoxin-AuIB), or alpha3/beta2 (alpha-conotoxin-MII) subunit interfaces to perturb respo

49 isine, (125)I-alpha-bungarotoxin, and (125)I-alpha-conotoxin MII) suggest the following: that alpha6b

50 these mutants revealed increased affinity of alpha-conotoxins MII, TxIA, and [A10L]TxIA at the alpha4

51 Structure-function analysis of alpha-conotoxin MII was performed in an attempt to gener

52 This peptide, named alpha-conotoxin MII, was identified by electrophysiologi

53 xin GIC shares some sequence similarity with alpha-conotoxin MII, which is also a potent alpha3beta2