ライフサイエンスコーパス: leak current

1 excitability via an increased GLT1b-mediated leak current.

2 generated by a calcium-inactivated potassium leak current.

3 desensitization to calcium of the potassium leak current.

4 ion is produced by blockade of an outward K+ leak current.

5 tentiation of glutamate-activated as well as leak currents.

6 and are thus dependent on persistent sodium leak currents.

7 all but significant changes in potassium and leak currents.

8 ive 5HT-induced currents and 5HT-independent leak currents.

9 urrent) that effectively acted as a negative leak current and counterbalanced the temperature-induced

10 y described hDAT conductances, including the leak current and the current associated with electrogeni

11 We also find that CA2 neurons have larger leak currents and more negative resting membrane potenti

12 TASK-1 carries a background or "leak" current and is a member of the two-pore domain pot

13 +), DAT displayed a cocaine-sensitive cation leak current approximately 10-fold larger than the subst

14 ion substrate, NIS exhibited a Na+-dependent leak current (approximately 35% of maximum substrate-ind

15 Second, Na(+)-mediated leak currents are eliminated.

16 temperatures, and subtraction of additional leak currents at elevated temperatures was sufficient to

17 application, which provides support for the leak current being mediated by GLT1b itself.

18 ange intracortical afferents or scaling K(+) leak current, but not several other Na(+) and K(+) intri

19 The Na(+) leak-current channel (NALCN) regulates locomotion, respi

20 -sulfonamide (NBQX)-sensitive portion of the leak current corresponded to a current generated by glut

21 Analysis of GluR1Lc leak current demonstrated that the 2,3-dioxo-6-nitro-1,2

22 alanine transport but still catalyzed anion leak current, demonstrating that substrate transport is

23 ntified a set of three maximal conductances (leak current, [Formula: see text]Leak; a persistent K cu

24 e) activates a NALCN channel-dependent Na(+)-leak current (I(L-Na)).

25 The native cerebellar granule neurone (CGN) leak current, IK(SO), is sensitive to block by zinc, wit

26 TC neurone, which contained only IT, Ih, K+ leak current (ILeak) and those currents responsible for

27 K+ outward currents: a voltage-independent 'leak' current (Ileak) operating at all negative potentia

28 es similarly augment the sustained K+ M- and leak-currents (IM and IK(L)).

29 and resulted in a 5-fold enhancement of the leak current in GLT1b-expressing oocytes with only a min

30 The leak current in Li(+) was also potently inhibited by low

31 ates, was modeled by the reduction in the K+ leak current in PY and TC cells and by a decrease in int

32 erefore, was effectively contributing to the leak current in the HN cells.

33 in isolated neural circuits due to increased leak currents in rhythm-generating neurons.

34 (A), I(K dr), I(Na), I(Ca L), I(Ca N), and I(leak) currents in postnatal cat RGCs.

35 The leak current increased slowly over 4 d of treatment with

36 The leak currents indicated that the mutated residues are ac

37 led the ability of IMI to reduce detrimental leak-current influences on neuronal networks over a broa

38 We propose that a nonspecific leak current introduced by the intracellular microelectr

39 he TTX- and Cs(+)-resistant background Na(+) leak current is absent in the mutant hippocampal neurons

40 tent sodium current (NaP) and K(+)-dominated leak current (Leak), primarily contribute to preMN/MN su

41 This leak current occurred in the absence of extracellular ca

42 Leak currents of different magnitudes appeared in the DI

43 By estimating the leak current parameters in regions in which there was li

44 hat persistent sodium (NaP) and K+-dominated leak currents primarily contribute to subthreshold I-V r

45 The epsilon subunit caused the appearance of leak currents recorded in the absence of GABA.

46 This result, and the small size of the leak current relative to the currents evoked by saturati

47 A depolarizing 'leak' current supports this firing pattern, but its mole

48 tudy demonstrated that ENaC mediates a Na(+) leak current that affects the steady state membrane pote

49 tor neurons, including a nonselective cation leak current that contributed to the resting potential,

50 ain (K(2P)) potassium channel that carries a leak current that is time- and voltage-independent.

51 batrin; 0.05-100 microm) resulted in a large leak current that was blocked by bicuculline (50 microm)

52 lase with semicarbazide (2 mm) decreased the leak current that was induced by vigabatrin by 47%.

53 Mutant Q185A receptors also had an increased leak current that was sensitive to picrotoxin, indicatin

54 2P) channels of the TREK subfamily generate 'leak' currents that regulate neuronal excitability, resp

55 d current, hDAT also mediates a constitutive leak current, the voltage and ionic dependencies of whic

56 3 alone reveals a constitutive, depolarizing leak current through hCHT.

57 and the upregulation of voltage-independent leak currents through a two-pore-domain potassium channe

58 of gating pores that were detected as proton leak currents through the VSDs.

59 sporter, we recorded the Na(+)-induced anion leak current to determine the K(m) of EAAC1 for Na(+).

60 The ATP1A1 mutations all caused inward leak currents under physiological conditions, and the CA

61 Dynamic clamp-mediated addition of leak currents was sufficient to stop neuronal oscillatio

62 Hyperpolarization-activated (IH) and leak currents were not altered during the application of

63 The leak currents were partially blocked by pentamidine but

64 K2P) channels are responsible for background leak currents which regulate the membrane potential and

65 sis to asparagine, Na(+) activated the anion leak current with a K(m) of about 2 m, indicating dramat