ライフサイエンスコーパス: intracellular solution

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1 avity becomes larger and contiguous with the intracellular solution.

2 binding sites to the extracellular or to the intracellular solution.

3 tivation peptides to enter the pore from the intracellular solution.

4 dition of 1.2 mM exogenous calretinin to the intracellular solution.

5 sodium-rich extracellular and potassium-rich intracellular solutions.

6 Omission of MgATP from the intracellular solution accelerated desensitization, and

7 st in ionic mixtures (like extracellular and intracellular solutions), and usually involve flow and t

8 tion of glibenclamide (10-100 microM) to the intracellular solution caused a concentration-dependent

9 Addition of genistein (100 microM) to the intracellular solution caused a small decrease in single

10 ATP currents activated by pinacidil when the intracellular solution contained 0.1 mM ATP.

11 Perfusion of a mock intracellular solution containing 0.22-0.23 microM Ca(2+

12 ive inhibition of MagNuM was accomplished by intracellular solutions containing 6 mM Mg.ATP, 1.2 mM f

13 Cells were perfused with mock intracellular solutions containing fluo 3.

14 he GABA(B) receptor antagonist CGP 55845 and intracellular solutions containing the GTP analog GDP-be

15 oss of endogenous ATP from the cell when the intracellular solution contains 0.3 mM ATP.

16 well approach with the ability for efficient intracellular solution exchange, describing protocols an

17 voltage paradigms and fast extracellular or intracellular solution exchange.

18 Sr2+ (200 microM), or reducing the pH of the intracellular solution from 7.2 to 6.2 did not block sus

19 lly inhibited by inclusion of heparin in the intracellular solution, indicating the involvement of mu

20 TRPM8 currents, and omission of ATP from the intracellular solution inhibited recovery from this inhi

21 e cytoplasmic components were replaced by an intracellular solution lacking any fast calcium buffer,

22 channel opening is higher when Mg2+ from the intracellular solution occupies its binding site.

23 Using intracellular solutions of physiological ionic compositi

24 show immediate and gradual effects of these intracellular solutions on measurement of the AHP and ba

25 in (300 nm) but was abolished in Cs(+)-based intracellular solution or during superfusion of 5 mm TEA

26 g-term recordings, which are affected by the intracellular solutions potassium methylsulphate (KMeth)

27 e (300 microM to 10 mM) in the patch pipette/intracellular solution prevented cADPR from evoking Ca2+

28 Acidification of the intracellular solution relieved channel block, suggestin

29 Acidification of the intracellular solution relieved glibenclamide inhibition

30 Removal of ATP and GTP from the intracellular solutions resulted in nearly complete tach

31 l patch electrodes filled with a Cs(+)-based intracellular solution to block the large-conductance Ca

32 he Glu203 residue delivers a proton from the intracellular solution to the core of ClC-ec1 via a rota

33 5-HT3 receptor as it could be recorded using intracellular solutions with or without adenosine tripho

34 ing/acidifying agents were mimicked by using intracellular solutions with pH directly buffered at hig

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