Sentence examples for membrane potential after from inspiring English sources

To evaluate the mitochondrial membrane potential after PDT, cells were stained using MitoTracker red CMXRos and Annexin-V FITC conjugated (both from Invitrogen).

The sensor measured the electric response of cultured membrane-engineered fibroblast cells suspended in an alginate gel matrix due to the change of their membrane potential after the interaction of the analyte molecules with the antibodies.

To this end, we investigated the effects on rapid depolarization and slow repolarization of the peritubular membrane potential after luminal addition of l-phenylalanine or l-alanine plus/minus KCNQ1 channel blockers.

Furthermore, due to the accelerated channel closing kinetics of this mutant, the recovery of the membrane potential after each spike was quicker as compared to neurons expressing wild-type Chrimson, leading to a more natural waveform of light-evoked action potentials (Supplementary Fig. 9c, d).

To examine the changes of membrane potential after cPAC exposure, the cells were stained with DiOC6(3,3′-dihexyloxacarbocyanineniodidedide) and then immediately analyzed using a flow cytometer.

Fig. 5 Imaging change of mitochondrial membrane potential after incubating free Dox and Dox-loaded TPP-NPs with A549 cells and Hela cells, the scale bar is 50 μm and applies to all parts.

In addition to the outward omega current, we identified an inward omega current over a range of negative membrane potentials, after a long depolarization of 1 min duration.

In addition to the outward omega current, we identified an inward omega pore current of 95 nS/nF at negative membrane potentials after long depolarizing pulses that shifts the R1242G residue above the omega pore constriction.

According to their effects and the binding sites on Nav channels: i) α-class scorpion toxins for Nav bind to channel receptor site 3 and show an effect in the inactivation mechanism of the channels [ 26, 27]; ii) Scorpion β-class toxins modify the Nav activation process by shifting activation to more negative membrane potentials after binding to site 4 [ 27- 29].

... We find that spike threshold depends logarithmically on Na channel density, and that Na channel inactivation and K channels can dynamically modulate it in an adaptive way: the threshold increases with membrane potential and after every action potential.

The membrane potential response after pairing was estimated by averaging over 80 trials.