ライフサイエンスコーパス: equilibrium potential

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

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

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

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

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

6 ls are exquisitely sensitive to the chloride equilibrium potential.

7 transport regulates cell volume and chloride equilibrium potential.

8 ing a hyperpolarization beyond the potassium equilibrium potential.

9 rsed polarity near the theoretical potassium equilibrium potential.

10 synaptic drive shifted toward the glutamate equilibrium potential.

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

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

13 -87.4 +/- 1.6 mV, which was close to the K+ equilibrium potential.

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

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

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

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

18 fication and reversed close to the potassium equilibrium potential.

19 in proteoliposomes by measuring transporter equilibrium potentials.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 25 neurons) that reversed polarity at the K+ equilibrium potential (n = 8 neurons) and was barium sen

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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