ライフサイエンスコーパス: extracellular potassium

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

2 rosporine treatment or through withdrawal of extracellular potassium.

3 sms underlying these events are dependent on extracellular potassium.

4 rdiac potassium channel that is modulated by extracellular potassium.

5 ition with acetazolamide, and independent of extracellular potassium.

6 ction) decreases sigmoidally with increasing extracellular potassium.

7 are responsible for NCC upregulation by low extracellular potassium.

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

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

10 erlies the mechanism of regulation of NCC by extracellular potassium.

11 rtant for physiological regulation of NCC by extracellular potassium.

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

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

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

15 withdrawal of depolarizing concentrations of extracellular potassium.

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

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

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

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

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

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

22 ed ULF currents could induce accumulation of extracellular potassium, accounting for the slowly devel

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

24 solely to sodium channel inactivation; (ii) extracellular potassium accumulation switches action pot

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

26 Low extracellular potassium activates NCC by decreasing intr

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

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

29 tors (AdRs) facilitates the normalization of extracellular potassium after acute photothrombotic stro

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

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

32 t engineered aldehyde reduction and elevated extracellular potassium and pH are sufficient to enable

33 The elevation of extracellular potassium and pH physically bolsters these

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

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

36 mulated changes in oxygenation, development, extracellular potassium, and temperature alter the preva

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

38 cted by recording the local field potential, extracellular potassium, as well as the intrinsic optica

39 Impaired extracellular potassium buffering has been proposed as o

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

41 systematically tested the effect of altered extracellular potassium, calcium, and sodium concentrati

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

43 Treating cells with elevated extracellular potassium caused membrane depolarization a

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

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

46 Elevation of extracellular potassium chloride resulted in spontaneous

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

48 Extracellular potassium concentration ([K(+)](e)) is kno

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

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

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

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

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

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

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

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

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

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

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

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

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

62 Extracellular potassium concentration affects the membra

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

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

65 ization characterized by a large increase of extracellular potassium concentration and prolonged subs

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

67 The increase in the extracellular potassium concentration associated with th

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

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

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

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

72 Extracellular potassium concentration increased during t

73 lar thermogenesis was detected by increasing extracellular potassium concentration to depolarize the

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

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

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

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

78 ere induced through repetitive elevations of extracellular potassium concentration.

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

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

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

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

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

84 rded at different temperatures and different extracellular potassium concentrations using the patch-c

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

86 High levels of extracellular potassium constrain T cell effector progra

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

88 nd NMDA receptors and the other dependent on extracellular potassium diffusion and persistent sodium

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

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

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

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

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

94 Depolarization with high extracellular potassium evokes Dpp release.

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

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

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

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

99 n of neurons in vivo and acute elevations of extracellular potassium in brain slices strongly decreas

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

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

102 Focal extracellular potassium increases in isolated Muller cel

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

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

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

106 Elevating extracellular potassium ion by 20 mM shifted the IC(50)

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

108 An increase of extracellular potassium ion concentration can result in

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

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

111 probably because of compensatory changes in extracellular potassium ions.

112 Extracellular potassium is a critical determinant of dru

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

114 ectly binds to and dephosphorylates NCC when extracellular potassium is elevated.

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

116 detect axonal activity through increases in extracellular potassium (K(+)) concentrations and activa

117 Glial regulation of extracellular potassium (K(+)) helps to maintain appropr

118 hat mild depolarization-mediated by elevated extracellular potassium (K(+))-induces a wide array of r

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

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

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

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

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

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

125 agonism facilitated the normalization of the extracellular potassium level after CSD, which parallele

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

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

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

129 ciated with highly reproducible increases in extracellular potassium levels in penumbra.

130 delayed response was not seen ex vivo where extracellular potassium levels were controlled by the pe

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

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

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

134 Extracellular potassium modulates recovery from C-type i

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

136 o slice preparations containing the preBotC, extracellular potassium must be elevated above physiolog

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

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

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

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

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

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

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

144 Decreased extracellular potassium promoted WNK4-RRxS phosphorylati

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

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

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

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

149 optosis in human keratinocytes is blocked by extracellular potassium supplementation, ZAKalpha knocko

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

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

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

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

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

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

156 e first time, to visualize intracellular and extracellular potassium transients during seizures in th

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

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

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

160 Extracellular potassium was found to have the largest bo

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

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

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

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

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

166 sease, and, therefore, selectively detecting extracellular potassium would allow the monitoring of di