ライフサイエンスコーパス: extracellular potassium

1 ompanied by a fast and sustained increase in extracellular potassium.

2 sms underlying these events are dependent on extracellular potassium.

3 rdiac potassium channel that is modulated by extracellular potassium.

4 urons with an activity-dependent increase of extracellular potassium.

5 by tetrodotoxin, ouabain, or the removal of extracellular potassium.

6 ng action potential wave form, and buffering extracellular potassium.

7 ssue under 4 mM (normal) and 8 mM (elevated) extracellular potassium.

8 ssing, and both were negated by elevation of extracellular potassium.

9 withdrawal of depolarizing concentrations of extracellular potassium.

10 rosporine treatment or through withdrawal of extracellular potassium.

11 , n=3), BaCl(2) (3 micromol/L, n=3), and low extracellular potassium (1 mmol/L, n=2) enhanced diastol

12 Exposure to elevated extracellular potassium (10, 20 and 40 mM K+) caused a d

13 age induced in CGNs by removing depolarizing extracellular potassium (5K apoptotic conditions), oxida

14 ine (norepinephrine; 10 microM), or elevated extracellular potassium (8 mM), could abruptly increase

15 e tested using a K(+) efflux inhibitor, high extracellular potassium, a mitochondrial reactive oxygen

16 Chronic increases in extracellular potassium, a signature of high neuronal ac

17 under physiologically relevant conditions of extracellular potassium accumulation during prolonged ac

18 de accumulation via the GABA(A) receptor and extracellular potassium accumulation via the K/Cl co-tra

19 ion was always associated with a decrease in extracellular potassium activity below baseline levels.

20 However, elevating extracellular potassium acutely after the period of acti

21 t recordings and propose a way of estimating extracellular potassium and activation of ATP-dependent

22 e block is voltage dependent, is relieved by extracellular potassium and has rapid kinetics, allowing

23 The elevation of extracellular potassium and pH physically bolsters these

24 termining glial contribution to buffering of extracellular potassium and uptake of potentially toxic

25 s are depolarized, in part because of raised extracellular potassium, and in part because of hypoperf

26 the mechanism(s) underlying the increase in extracellular potassium, and the different time courses

27 Impaired extracellular potassium buffering has been proposed as o

28 d AHPs were blocked by ouabain or removal of extracellular potassium, but not by intracellular calciu

29 zation of inhibitory terminals with elevated extracellular potassium caused a large increase in the f

30 Treating cells with elevated extracellular potassium caused membrane depolarization a

31 ld potentials, intracellular activities, and extracellular potassium changes demonstrates that SLEs i

32 MEF2A protein was sensitive to the level of extracellular potassium chloride (KCl) and depolarizing

33 Elevation of extracellular potassium chloride resulted in spontaneous

34 epolarization tendency at normal and reduced extracellular potassium compatible with the diagnosis.

35 on (APD) can be further enhanced by lowering extracellular potassium concentration ([K(+)](o)) from 5

36 hannel Kir4.2 is sensitive to changes in the extracellular potassium concentration ([K(+)](o)).

37 Elevation of the extracellular potassium concentration ([K(+)]e) impairs

38 persisting effects of depolarizing rises in extracellular potassium concentration ([K+](o)) on synap

39 in intracellular and extracellular pH evoked extracellular potassium concentration ([K+]o were record

40 ously recorded together with measurements of extracellular potassium concentration ([K+]o) and a tran

41 The effects of raising extracellular potassium concentration ([K+]o) from 3.0 t

42 outward currents such as I(Kr) or I(Kl) when extracellular potassium concentration ([K+]o) is increas

43 ission is depressed by moderate rises in the extracellular potassium concentration ([K+]o).

44 During neuronal activity, extracellular potassium concentration ([K+]out) becomes

45 gle-channel conductance was dependent on the extracellular potassium concentration ([K]o).

46 RP cells were depolarized by ACh and by high extracellular potassium concentration (high K(+)).

47 ompanied by increases (0.5 to 2.0 mM) in the extracellular potassium concentration [K+]o.

48 imulation was associated with an increase in extracellular potassium concentration and neuronal depol

49 es astrocyte potassium buffering, increasing extracellular potassium concentration and overactivating

50 c brain injury (TBI) can be predicted by the extracellular potassium concentration and the change in

51 The increase in the extracellular potassium concentration associated with th

52 Astrocytes are thought to regulate the extracellular potassium concentration by mechanisms invo

53 chanisms-namely, the effects of an increased extracellular potassium concentration diffusing in space

54 s coincident with a stimulus-induced rise in extracellular potassium concentration during stimulation

55 thought to be critical for the buffering of extracellular potassium concentration in retina.

56 Extracellular potassium concentration increased during t

57 cular (AV) node is insensitive to changes in extracellular potassium concentration, [K+]o, because of

58 ed in a Nernstian manner with changes in the extracellular potassium concentration.

59 hifted in a Nernstian manner with changes in extracellular potassium concentration.

60 was a function of membrane potential and the extracellular potassium concentration.

61 ere induced through repetitive elevations of extracellular potassium concentration.

62 of extracellular Ca(2+) and depended on the extracellular potassium concentration.

63 extracellular space, and an increase in the extracellular potassium concentration.

64 n-mediated transcription induced by lowering extracellular potassium concentration.

65 Seizures coincide with an increase in extracellular potassium concentrations [K(+)](e) yet lit

66 ently reported that the presence of abnormal extracellular potassium concentrations in tumors suppres

67 nock-out mice under both normal and elevated extracellular potassium conditions.

68 sthetized rat hippocampus suggested that the extracellular potassium could play an important role in

69 We therefore predict that extracellular potassium dynamics can cause alternating e

70 tational model of a neocortical circuit with extracellular potassium dynamics to show that activity-d

71 To test the hypothesis that extracellular potassium elevation also alters the stimul

72 We explored the effect of mild extracellular potassium elevation to increase hippocampa

73 nts and mathematical modeling indicates that extracellular potassium emitted from the biofilm alters

74 Depolarization with high extracellular potassium evokes Dpp release.

75 t several processes, including regulation of extracellular potassium, glucose storage and metabolism,

76 ionic species, with intracellular sodium and extracellular potassium having discordant gradients, fac

77 Short-term synaptic plasticity and extracellular potassium homeostasis during neural excita

78 ts reversal potential shifted with change of extracellular potassium in agreement with the value pred

79 form of randomly timed IPSCs (evoked by high extracellular potassium) in high-frequency OHCs is alter

80 Fast-rising and sustained extracellular potassium increases associated to interneu

81 Focal extracellular potassium increases in isolated Muller cel

82 In this study, brain extracellular potassium ion activity and local cerebral

83 to a greater degree in hyperthermic animals, extracellular potassium ion activity showed delayed seco

84 No secondary elevation of extracellular potassium ion activity was observed in hyp

85 rfused in vitro with normal Tyrode solution (extracellular potassium ion concentration 4 mmol/liter)

86 An increase of extracellular potassium ion concentration can result in

87 ity-dependent, transient variations of local extracellular potassium ion concentration in the central

88 ances such as ischemia and hyperkalemia, the extracellular potassium ion concentration is elevated.

89 probably because of compensatory changes in extracellular potassium ions.

90 Extracellular potassium is a critical determinant of dru

91 der ionic conditions that favor efflux, when extracellular potassium is elevated and the sodium gradi

92 Using BHK cells, removal of extracellular potassium (K(+)) caused yellow fluorescent

93 Here we show that modest elevation of extracellular potassium (K+) activated inward rectifier

94 ar calcium ([CA2+]i), intracellular pH (pHi) extracellular potassium ([K+]e), extracellular pH (pHe),

95 ellular space (ECS) to cellular K+ efflux on extracellular potassium ([K+]o) accumulation in response

96 the role of astrocytes in the regulation of extracellular potassium ([K+]o) and calcium ([Ca2+]o) le

97 fferences in outward current profiles and in extracellular potassium ([K+]o) dependence.

98 s study, we evaluated the effect of changing extracellular potassium ([K+]o) on IKr block by the nons

99 n biology, and quantitative detection of the extracellular potassium level is important.

100 In Toxoplasma gondii, extracellular potassium levels and other stimuli trigger

101 KCC2 regulates intraneuronal chloride and extracellular potassium levels by extruding both ions.

102 t caspase-1 activation was inhibited by high extracellular potassium levels, whereas Ipaf-dependent a

103 d with GTs after reverse-dialysis to elevate extracellular potassium levels.

104 are induced to undergo apoptosis by lowering extracellular potassium, MEF2A and MEF2D are phosphoryla

105 Extracellular potassium modulates recovery from C-type i

106 l cultures, chronic depolarization with high extracellular potassium moves multiple components of the

107 Here we show that high extracellular potassium opens pannexin channels leading

108 rm activity was elicited by either increased extracellular potassium or 4-AP.

109 xtracellular sodium concentration but not on extracellular potassium or chloride concentration.

110 ellular calcium levels with chronic elevated extracellular potassium or with the calcium channel agon

111 observed that tetraethylammonium (TEA), high extracellular potassium, or cysteine protease inhibitors

112 erent in that cardiac tissue shows a rise in extracellular potassium over several minutes from about

113 keletal muscle fibres in response to reduced extracellular potassium, owing to an inward cation-selec

114 NPY induced a current that was dependent on extracellular potassium, reversed near the potassium equ

115 re preceded by outward currents coupled with extracellular potassium shifts, abolished by pharmacolog

116 ytes with the NLRP3 inhibitor MCC950 or with extracellular potassium significantly reduced IL-1beta c

117 moved by trypsin and prolonged by decreasing extracellular potassium suggest that the blocking partic

118 t was accompanied by a transient increase in extracellular potassium that diffused across the lesion.

119 For 8-mM extracellular potassium, the break or stimulus terminati

120 of rubidium efflux increased with increasing extracellular potassium: the t(1/2) at 50mM potassium wa

121 rictal bursting was observed on elevation of extracellular potassium to 6.5 mM, a condition that resu

122 al rise followed by a very rapid increase in extracellular potassium to levels of 50-80 mM.

123 f Kv1.3 can be accelerated by the binding of extracellular potassium to the channel in a voltage-depe

124 ermining the magnitude of single-spike local extracellular potassium transients, is a basic determini

125 ersal potentials, is regulated together with extracellular potassium via kation chloride cotransporte

126 for IK(IR) measured in 6, 12, 60 and 140 mM extracellular potassium was a function of membrane poten

127 Extracellular potassium was found to have the largest bo

128 After seizure termination, the extracellular potassium was reduced below baseline, resu

129 uency was primarily achieved by manipulating extracellular potassium, which significantly affects neu

130 ischemia can be explained by an increase in extracellular potassium, while the increase during reper

131 ents, and ERG blockade impaired clearance of extracellular potassium with little direct effect on hip

132 Stimulating secretion with elevated extracellular potassium, with the calcium ionophore iono