ライフサイエンスコーパス: bath solution

1 e nature of the counter cation in the oocyte bath solution.

2 in the absence and presence of Cd(2+) in the bath solution.

3 was prevented when NFPS was included in the bath solution.

4 x is formed when fluo-3 meets calcium in the bath solution.

5 din (25--75 microg ml(-1)) in HCO(3)(-)-free bath solution.

6 xchange system in equilibrium with a uniform bath solution.

7 s were obtained when tetrodotoxin was in the bath solution.

8 ibited by addition of 10 microM Oxo-M to the bath solution.

9 ited KATP channel activity when added to the bath solution.

10 or GTP and ATP (1 mmol/L) were added to the bath solution.

11 d either through the patch pipette or in the bath solution.

12 ng pipette and with metabolic poisons in the bath solution.

13 .5 mM EGTA) or addition of 10 mM Co2+ to the bath solution.

14 s were perfused with identical perfusate and bath solutions.

15 the response to changes in osmolality of the bathing solution.

16 hed by removing Na(+) from the extracellular bathing solution.

17 EG) or by lowering the ionic strength in the bathing solution.

18 ted by adding and removing mannitol from the bathing solution.

19 polyanionic dextran sulfate to the membrane bathing solution.

20 when cells were perfused with a Ca(2+)-free bathing solution.

21 +) with BAPTA or by omitting Ca(2+) from the bathing solution.

22 ed when cells were incubated in a hypertonic bathing solution.

23 vitro application of losartan to the serosal bathing solution.

24 by adding mannitol (50 or 100 mmol/l) to the bathing solution.

25 igh [Ca2+]i induced by empirically optimized bathing solutions.

26 in the presence of calyculin A (1 microM in bath solution), a membrane permeant inhibitor of phospha

27 enhanced the sensitivity of isolated TRCs to bath solution acidification due to activation of the PA

28 ed significantly in CaM-enriched (20 microM) bath solution and this effect was prevented by a specifi

29 nsion-dependent exchange of MOPC between the bathing solution and the membrane.

30 icantly increased calcium currents in normal bathing solutions and during exposure to 110 mM BaCl(2)

31 (ASIC) blocker amiloride, absent in Na+-free bathing solution, and enhanced by either Ca2+-free buffe

32 As the ion concentrations in the bath solution are systematically varied, the ion content

33 tes were deformed with pneumatic ejection of bath solution at 5-15 psi using a glass pipette (7-15 mi

34 r of voltage-dependent Ca2+ channels, to the bath solution blocked the stimulatory effects of glutama

35 y activating current was reduced in Na+-free bathing solution but enhanced when the extracellular K+

36 (2+) exchanger (NCX) via alkalization of the bath solution, by adding lanthanum, or by substitution o

37 annel-impermeable N-methyl-D-glucamine-based bath solutions, consistent with increases in the Na(+) t

38 When both bathing solutions contain equimolar concentrations of li

39 The bath solution contained APV, CNQX and bicuculline to blo

40 nsport experiments (S(2) segments only), the bathing solution contained 2.3 microM (3)H-GSH.

41 d for 4-16 h with 5-HT and then exposed to a bath solution containing 10 microM forskolin.

42 saicin or 1.6 microm resiniferatoxin using a bathing solution containing 10 microm Ruthenium Red (to

43 f 50 nM antiPGE2 antibody to the basolateral bathing solution decreased basal Isc by 20 % and shifted

44 io)triphosphate (100 mum) to the cytoplasmic bathing solutions decreased the activity of the ORCC and

45 r PEG, addition of the crown to the membrane-bathing solution decreases the ionic conductance of the

46 pipette solution, addition of steroid to the bath solution dramatically shifted the steroid potentiat

47 When added to the bath solution, each of these neuromodulators produced a

48 at pungent chemicals added to the pipette or bath solution easily activated TRPA1 in cell-attached pa

49 moval of CO(2)/HCO(3)(-) from the blood-side bathing solution elicited a approximately 50% reduction

50 was omitted or substituted for Sr(2+) in the bath solution, if neurons were treated with carbonylcyan

51 In a normal bathing solution in which muscle nicotinic receptors wer

52 Addition of 5 mM L-alanine to the bathing solution increased the whole cell conductance an

53 This then slowly decreased as the bathing solution increased to 1000 mM.

54 Removal of glucose from the bath solution induced this inward current within 50 +/-

55 f nanomolar concentrations of peptide in the bathing solution induced a transmembrane conductance tha

56 uced by negative osmotic pressure (hypotonic bath solutions) induced a large outwardly rectifying Cl-

57 h Mg(2+) and Co(3+)Hex concentrations in the bath solution, it is observed that the spacing is largel

58 c mGluR5 antagonist, MPEP was applied in the bath solution, LTP was enhanced in layer VI, and blocked

59 specific mGluR1 antagonist, LY367385, to the bath solution, LTP was reduced in layer II/III and layer

60 wide variety of voltage clamp protocols and bathing solution manipulations.

61 of actin or protein kinase A plus ATP to the bathing solution of excised inside-out patches.

62 ubules were bathed in 16% sucrose-containing bath solution or treated with concanavalin A.

63 and generated by removal of Mg(2+) from the bathing solution or by raising extracellular K(+) from 3

64 nd after either changes in osmolarity of the bathing solutions or the additions of amphotericin B, ep

65 ) instead of Ca(2+), (iii) using Ca(2+)-free bath solution, or (iv) buffering [Ca(2+)](i) with BAPTA-

66 rrent was reduced by removing Na(+) from the bath solution, or by knocking down levels of Slack using

67 Removal of Ca2+ from the bathing solution, or the addition of 0.1 mM Cd2+ complet

68 Lowering bath solution pH diminished the inhibition by Cu(2+).

69 ) by increased proton concentration when the bathing solution pH is less than 3.

70 presence of a NMDA antagonist, D-AP5, in the bath solution, potentiation was blocked in layer II/III,

71 Replacement of Na+ with K+ ions in the bathing solution produced a shift in reversal potential

72 (S)-3,5-dihydroxyphenylglycine (DHPG) to the bathing solution, pyramidal cells initially firing regul

73 microM diC8-PIP(2) in the patch pipette and bathing solutions, respectively, inhibited angiotensin I

74 -5 micro M of either of them to the membrane bathing solutions resulted in formation of long-lived an

75 Increases in chloride ion levels in the bathing solution results in chloride extraction and liga

76 Addition of H(2)O(2) into the bath solution significantly increased the probability of

77 s not restored by adding excess BAPTA to the bathing solution, so as to reverse the Ca2+ gradient.

78 presence of isosmolar luminal perfusate and bath solutions, spontaneous fluid absorption rates (nl/m

79 Cell swelling induced by hyposmotic bath solution stimulated Cl(-) currents in arterial myoc

80 d by hyposmotic (250 osmol (l solution)(-1)) bath solution stimulated Gd(3+)-sensitive ICat in smooth

81 2P channels are more profound in Na(+)-based bath solutions than in channel-impermeable N-methyl-D-gl

82 is only released 13.6-fold more calcium into bathing solutions than C. communis.

83 -HT and halothane were examined in acidified bath solutions that blocked TASK channels.

84 owing a fast switching of a low Na(+) (1 mm) bath solution to a high Na(+) (110 mm) solution.

85 Reduction of [ATP] in the bathing solution to 0.5 and 0.2 mM ATP progressively dec

86 found in a nominally Ca(2+)-free/high-Mg(2+) bath solution using cell-attached recording.

87 After a period of baseline measurements, the bathing solution was changed either to one of identical

88 When temperature of the bathing solution was increased to 39 degrees C, CSQ1-kno

89 When sodium chloride in the bathing solution was replaced isosmotically with choline

90 MM) in the range 20-511 kDa, added to the TM bathing solution was used to exert an osmotic pressure.

91 ver that amplifies currents in divalent-free bath solutions, we show that EC CRAC has similar charact

92 Perfusion and bathing solutions were iso-osmotic Cl-free Ringer's solu

93 r, 30 microm La(3+), but were abolished in a bath solution when Ca(2+) was omitted.

94 ide-out patches to a carbon monoxide-bubbled bath solution, which increased channel activity.

95 ut patches was increased by perfusion of the bath solution with 30 microm PIP(2) plus 100 microm GTP

96 Here we show that in Na(+)-based bath solutions with physiological K(+) gradients, lowere

97 ently reduced ICl,vol in Ca2+-free hypotonic bath solutions with strong intracellular Ca2+ (Ca2+i) bu

98 In Ca2+-containing hypotonic bath solutions with weak Ca2+i buffering, however, isopr

99 Buffering the bathing solutions with EGTA to reduce the free [Ca(2+)]