ライフサイエンスコーパス: N-methyl-D-glucamine

1 effect in Na(+)-depleted cells (replaced by N-methyl-d-glucamine).

2 r by replacement of extracellular Na(+) with N-methyl-d-glucamine.

3 etrodotoxin or by replacement of sodium with N-methyl-d-glucamine.

4 ductance, rectification, and permeability of N-methyl-d-glucamine.

5 Na+ was replaced with an impermeant cation, N-methyl-D-glucamine.

6 allows permeation of larger cations such as N-methyl-d-glucamine.

7 ferent substrates to be Na+, 1 > Cl-, 0.34 > N-methyl-D-glucamine, 0.27 > L-glutamate, 0.15 approxima

8 ic Cl-free Ringer's solutions modified using N-methyl-D-glucamine and cyclamate as the Na and Cl subs

9 by substitution of extracellular Na(+) with N-methyl-d-glucamine and inhibited by flufenamic acid (5

10 largely impermeant ions (tetraethylammonium, N-methyl-D-glucamine and methanesulphonate) and was augm

11 ic monovalent cations tetraethylammonium and N-methyl-D-glucamine are much less permeant.

12 A wide variety of monovalent cations (TEA, N-methyl-D-glucamine, arginine, choline, CH3NH3+, Li+, C

13 he ion selectivity series lithium > sodium > N-methyl-d-glucamine at pH 7.4.

14 d bath solutions than in channel-impermeable N-methyl-D-glucamine-based bath solutions, consistent wi

15 Replacing external Na+ with N-methyl-D-glucamine, blocking Ca2+ entry, or preventing

16 ) can also permeate truncated pumps, whereas N-methyl-D-glucamine cannot.

17 ermeant ions (Ca(2)(+) and Na(+) replaced by N-methyl-d-glucamine), Cd(2)(+) carried sizable inward c

18 ect was reversed by replacement of NaCl with N-methyl D-glucamine chloride.

19 ause substitution of extracellular NaCl with N-methyl-D-glucamine chloride completely blocked the rel

20 BTP2 still blocked TRPC3 in medium with N-methyl-D-glucamine-chloride replacing Na+, indicating

21 Recovery rates in N-methyl-D-glucamine+ Cl- or in 0.25 M sucrose are not s

22 but not abolished by substitution of either N-methyl-D-glucamine- Cl(-) or tetramethylammonium for N

23 Partial Na+ substitution by N-methyl-D-glucamine completely abolished this residual

24 lacement of extracellular Na with impermeant N-methyl-D-glucamine decreased its amplitude and shifted

25 ce, whereas choline, tetraethylammonium, and N-methyl-D-glucamine did not.

26 red radical using the spin traps of iron(II) N-methyl-D-glucamine dithiocarbamate [(MGD)2-FeII] and 5

27 ons from nitrite in the presence of the iron-N-methyl-D-glucamine dithiocarbamate complex ((MGD)(2)Fe

28 In the presence of the NO trap Fe2+-N-methyl-D-glucamine dithiocarbamate, NO gives rise to c

29 Addition of N-methyl-D-glucamine dithiocarbamate-Fe solution, an NO-

30 fusion of membrane-impermeable NO scavengers N-methyl-D-glucamine dithiocarbamate/ferrous sulfate mix

31 synthase (NOS) incubated with the spin trap N-methyl-D-glucamine-dithiocarbamate-FeII produced a sig

32 of Ip was largely reduced by substitution of N-methyl-D-glucamine+ for external Na+, the magnitude of

33 y the replacement of extracellular sodium by N-methyl-D-glucamine in the presence of TTX, with correc

34 oride and substitution of all Na+ with NMDG (N-methyl-D-glucamine) in the apical solution.

35 rably selective to Na(+), K(+), choline, and N-methyl-D-glucamine, indicating a fairly large, poorly

36 ce of intracellular organic cations (such as n-methyl-D-glucamine) induces a pronounced negative shif

37 Replacement of extracellular Na(+) with N-methyl-D-glucamine inhibited I(LVA) and shifted the re

38 In the presence of N-methyl-D-glucamine(+), NMDA instantly hyperpolarized t

39 Replacing Na(+) with N-methyl-d-glucamine (NMDG(+)) did not reduce the affini

40 P2X7 receptor currents carried by Na(+) and N-methyl-D-glucamine (NMDG(+)) showed enhanced activatio

41 passage of larger synthetic cations, such as N-methyl-d-glucamine (NMDG(+)).

42 was permeable to calcium (PCa/PNa = 1.5) and N-methyl-d-glucamine (NMDG) (PNMDG/PNa = 0.4); it was al

43 tials were measured in extracellular sodium, N-methyl-D-glucamine (NMDG) and NMDG containing 5 mM Ca2

44 Replacement of Na+ with choline or N-methyl-D-glucamine (NMDG) and of Cl- with sulfate or g

45 of all extracellular monovalent cations, by N-methyl-D-glucamine (NMDG) substitution, eliminated OCs

46 When external sodium was replaced by N-methyl-D-glucamine (NMDG) with TTX present, cells hype

47 ity of K approximately equal to Na >> Tris > N-methyl-D-glucamine (NMDG), and is blocked by high conc

48 a+ in the hypotonic buffer was replaced with N-methyl-D-glucamine (NMDG), RVD in the presence of MeHg

49 the presumably NMDA channel-impermeant ions N-methyl-D-glucamine (NMDG), Tris or sucrose.

50 reased permeability to large cations such as N-methyl-D-glucamine (NMDG).

51 no activity is observed with Na(+), Li(+) or N-methyl-D-glucamine (NMDG).

52 lar Na+ was replaced by TEA or Tris, but not N-methyl-D-glucamine (NMDG).

53 When external Na+ ions were replaced by N-methyl-D-glucamine (NMDG+) NFA still enhanced I(Cl(Ca)

54 pands to accommodate large molecules such as N-methyl-D-glucamine (NMDG+).

55 e observed when Na(i,o)(+) was replaced with N-methyl-D-glucamine (NMG(+))(i, o).

56 was maintained by replacement of [Na+] with N-methyl-d-glucamine (NMG+), suggesting that the enhance

57 In normal ionic strength (120 mM N-methyl-D-glucamine, NMG), La3+ blocked the current wit

58 Replacement of extracellular sodium with N-methyl-D-glucamine or choline caused a fall in [Cl-]i

59 acement of all extracellular Na+ with either N-methyl-D-glucamine or choline chloride increased the E

60 at do not support the NaCaX operation, i.e., N-methyl-D-glucamine(+) or Li(+), on: PM potential; cyto

61 ation, replacing external cations with NMDG (N-methyl-D-glucamine) or by addition of 10 mM caesium or

62 ately 50% of extracellular Na+ with Tris+ or N-methyl-D-glucamine reduced or eliminated the response.

63 ntrations of Cs glutamate, L-arginine Cl, or N-methyl-D-glucamine significantly increased both the re

64 and PPADS, and it permeated the large cation N-methyl-d-glucamine upon activation.

65 N-Methyl-D-glucamine was finitely permeant.