ライフサイエンスコーパス: equilibrium potential

1 rmate with high Faradaic efficiency near the equilibrium potential.

2 channels hyperpolarizes the cell to the K(+) equilibrium potential.

3 ting in a depolarizing shift of the chloride equilibrium potential.

4 potential and is reversed upon return to the equilibrium potential.

5 ance with a reversal potential near the K(+) equilibrium potential.

6 t had a reversal potential close to the K(+) equilibrium potential.

7 he OT-sensitive current reversed at the K(+) equilibrium potential.

8 icant rate at very small deviations from the equilibrium potential.

9 ls are exquisitely sensitive to the chloride equilibrium potential.

10 transport regulates cell volume and chloride equilibrium potential.

11 ing a hyperpolarization beyond the potassium equilibrium potential.

12 rsed polarity near the theoretical potassium equilibrium potential.

13 synaptic drive shifted toward the glutamate equilibrium potential.

14 ent, CLT-sensitive, and reversed near the K+ equilibrium potential.

15 -87.4 +/- 1.6 mV, which was close to the K+ equilibrium potential.

16 rameter; and (2) a positive change in the K+ equilibrium potential.

17 receptor antagonists and reverse at the Cl- equilibrium potential.

18 t in the reversal potential to the potassium equilibrium potential.

19 panied by an 8 mV depolarization in the IPSP equilibrium potential.

20 fication and reversed close to the potassium equilibrium potential.

21 in proteoliposomes by measuring transporter equilibrium potentials.

22 follows: 1) comparison of V(rev) with proton equilibrium potential; 2) measurement of pH(in) and V(re

23 larized (-55 +/- 2 mV) relative to the Cl(-) equilibrium potential (-24 mV) during muscarinic stimula

24 y depolarizations that approached the Ca(2+) equilibrium potential and by treatments that blocked Ca(

25 epsilon subunit reversed in sign at the Cl- equilibrium potential and exhibited outward rectificatio

26 The influence of nanocrystal size on the equilibrium potential and kinetics of Li insertion is in

27 lling-activated current shifted with the Na+ equilibrium potential and not the Cl- equilibrium potent

28 (Vm) would quickly (<1 ms) reach the Ca(2+) equilibrium potential and SR Ca(2+) release would cease.

29 ent widening the difference between the K(+) equilibrium potential and the E(M).

30 mechanism instead suggests that the Li/Li(+) equilibrium potential and the surface energy-thermodynam

31 tration dependent, reversed at the potassium equilibrium potential and was blocked by BaCl2 , charact

32 current that reversed near the predicted K+ equilibrium potential and was not affected by changes in

33 ed by Erev >= ECl (where ECl is the chloride equilibrium potential) and partial blockade by extracell

34 lular responsiveness, reversed near the K(+) equilibrium potential, and was prevented by intracellula

35 For a benzimidazole-based hydride donor, HRR equilibrium potentials are roughly invariant across solv

36 Donnan effects, osmotic pressure and Donnan equilibrium potentials, are significantly amplified, whi

37 In K+-free conditions with the chloride equilibrium potential at about -50 mV, intracellular app

38 the resting membrane potential and the GABA equilibrium potential became more hyperpolarized with ti

39 current reversal near the expected chloride equilibrium potential, current sensitivity to the anion

40 nsity of the metal film increased, while the equilibrium potential decreased with increasing solid fi

41 fference between their average value and the equilibrium potential defines the directionality (also c

42 receptors, which, due to the positive anion equilibrium potential, depolarizes chromaffin cells.

43 tic inhibition with a physiological chloride equilibrium potential (E(Cl)) (-75 mV) fails to hyperpol

44 The slow current reversed near the Cl(-) equilibrium potential (E(Cl)) and was reduced by anthrac

45 al of I(Cl(Ca)) was close to the theoretical equilibrium potential (E(Cl)) and was shifted by replace

46 epolarize, depending on whether the chloride equilibrium potential (E(Cl)) is negative or positive, r

47 r chloride and, therefore, a depolarized Cl- equilibrium potential (E(Cl)).

48 ellular Cl(-) levels and a depolarized Cl(-) equilibrium potential (E(Cl)).

49 ard Cl- flux and causes a more negative GABA equilibrium potential (E(GABA)) in immature neurons.

50 t reversed at a potential close to the Na(+) equilibrium potential (E(Na)), and replacing Na(+) with

51 This is due to more depolarized GABA(A)R equilibrium potentials (E(GABAAR)), which are shown to r

52 timulated a current that reversed near Cl(-) equilibrium potential, E(Cl).

53 rge contractions at potentials near the Ca2+ equilibrium potential (ECa).

54 Changing the chloride equilibrium potential (ECl) from 0 to +27 mV shifted the

55 esulted in a large negative shift in the Cl- equilibrium potential (ECl) that attenuated the GABA-med

56 t effects of IPSP generation is the chloride equilibrium potential (ECl).

57 thane current reversed near the predicted K+ equilibrium potential (EK) and was reduced in elevated e

58 a null potential close to the calculated K+ equilibrium potential (EK) of -110 mV.

59 The K+ equilibrium potential (EK) was more negative than Em in

60 l close to or negative to the theoretical K+ equilibrium potential (EK), -94 mV, in 8/17 neurones; ty

61 ersal potential that was dependent on the K+ equilibrium potential (EK).

62 , [Na+]i was 12-13 mM corresponding to a Na+ equilibrium potential (ENa) of about 58 mV.

63 The Na+ equilibrium potential (ENa) was positive in the trophobl

64 The equilibrium potential (Er) for the depolarization was li

65 re-activated by brief pulses to +120 mV (the equilibrium potential for Ca2+, ECa), followed by steps

66 ents at membrane potentials above the Nernst equilibrium potential for Cl(-) and thus can be used as

67 y rectifying currents that reversed near the equilibrium potential for Cl(-) ions (E(Cl)).

68 nnels and clamps membrane potential near the equilibrium potential for Cl(-) ions.

69 Using an estimate of the equilibrium potential for CO(2) reduction to CO under op

70 ulness results in depolarizing shifts in the equilibrium potential for GABA(A) receptors, reflecting

71 steady-state current that reversed near the equilibrium potential for K(+) and voltage-dependently a

72 s since it had a reversal potential near the equilibrium potential for K(+), was inhibited by the K(A

73 se responses closely approximated the Nernst equilibrium potential for K(+).

74 ectifying with a reversal potential near the equilibrium potential for K+ ions, and is suppressed by

75 oss command potentials and reversed near the equilibrium potential for K+ ions.

76 ard current that reversed near the estimated equilibrium potential for K+, indicating the depolarizat

77 these two ionic conditions were close to the equilibrium potential for K+, suggesting K+ selectivity.

78 and the reversal potential was close to the equilibrium potential for K+.

79 rd current was close to the predicted Nernst equilibrium potential for Na+.

80 ive neurotransmitter current reversed at the equilibrium potential for potassium (E(K)) and displayed

81 ween oxidation and reduction) sharply at the equilibrium potential for the substrate redox couple.

82 The equilibrium potentials for TEA(*) and TEOA(*) were deter

83 Reversal potentials were close to equilibrium potentials for transmembrane pH gradients an

84 ance is present, the only way to keep the Cl-equilibrium potential in accordance with the changed mem

85 chloride indeed hyperpolarized the chloride equilibrium potential in MNs and increased reciprocal in

86 olarized by approximately 4 mV from the K(+) equilibrium potential, indicating that background K(+) c

87 he Na+ equilibrium potential and not the Cl- equilibrium potential, indicating that the swelling-acti

88 When this positive change to the K(+) equilibrium potential is combined with the blockage of r

89 C soma and distal dendrites if (1) the Cl(-) equilibrium potential is more positive in the proximal d

90 lized through quantifying the underlying non-equilibrium potential landscape topography and the kinet

91 25 neurons) that reversed polarity at the K+ equilibrium potential (n = 8 neurons) and was barium sen

92 ceptors and found that the hallmark shift in equilibrium potential observed with prolonged channel ac

93 ustains MHb depolarization near the chloride equilibrium potential of -30 millivolts, thereby enablin

94 ifted to -76 mV, closer to the estimated Cl- equilibrium potential of -56 mV, while that of the inwar

95 activity causes a positive shift in the HER equilibrium potential of 71 mV.

96 The chloride equilibrium potential of bipolar cells was found to be n

97 rrent was found to reverse at -3 mV when the equilibrium potential of Cl- (ECl) was -2 mV, and the re

98 basis for this appears to be a change in the equilibrium potential of GABA-evoked current.

99 ogen chloride solution, is very close to the equilibrium potential of hydrogen.

100 aused by temperature-dependent shifts of the equilibrium potential of Li(0)/Li(+) Supported by simula

101 ead of ca. -0.65 V for 2), very close to the equilibrium potential of NAD(+)/NADH redox couple (E deg

102 e, despite the well known depolarizing Cl(-) equilibrium potential of neonatal hippocampal neurons, p

103 e reduction potential is finely tuned to the equilibrium potential of the H(+)/H(2) couple, the poten

104 als has been shown to be equal to the Nernst equilibrium potential of the most permeant inorganic ion

105 on efflux at voltages between -50 mV and the equilibrium potential of the prevailing anion; and (c) a

106 After excitatory blockade, the apparent equilibrium potential of the rhythmic synaptic drive shi

107 We also measured changes in the apparent equilibrium potential of the rhythmic, synaptic drive of

108 In the presence of bicuculline, the apparent equilibrium potential of the synaptic drive shifted towa

109 e-channel currents reversed at 0 mV when the equilibrium potentials of all ions present were far from

110 ge state are facilitated using values of the equilibrium potentials of these transitions, as well as

111 of the current closely followed the hydrogen equilibrium potential over a wide range of internal-exte

112 fference between membrane voltage and the K+ equilibrium potential rather than on membrane voltage it

113 hesizing value-added chemicals over the near equilibrium potential regime, i.e., formate production o

114 detected using this method since the overall equilibrium potential response of polyions increases wit

115 lular potassium, reversed near the potassium equilibrium potential, showed inward rectification, was

116 ents at membrane voltages negative to the K+ equilibrium potential than outward currents at voltages

117 tration in neurons below its electrochemical equilibrium potential, thus favoring robust GABA hyperpo

118 ersal potential (Erev) was -31 +/- 3 mV with equilibrium potential values for C1- (EC1) and Na+ (ENa)

119 es of IK,L were affected by an unstable K(+) equilibrium potential (Veq K(+) ).

120 brane potential which followed the potassium equilibrium potential when [K+]o was raised.

121 n in response to even a small departure from equilibrium potential, with a catalytic bias for the for

122 ed to a 24 mV depolarizing shift in the IPSC equilibrium potential within 1 d of deafferentation.

123 cit representation of Na(+), K(+), and Ca(2+)equilibrium potentials, yet mathematical simplicity is r