Effects of Low Power 2450MHz Magnetic Field on Characteristics of Delayed Rectifier Potassium Current of Cortical Neurons

Zhang, Yang; Yu, Zheng; Wang, Jinhai; Zhang, Zizhao; Yue, Wei; Liu, Gengbo

doi:10.1109/icbeb.2012.185

Cited by 1 publication

(1 citation statement)

References 8 publications

(6 reference statements)

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“…In all experiments, the cells were stabilized for 2-3 min after the cell membrane was broken, then the data before and 5 min after drug perfusion were recorded, and the data were recorded after 5 min of drug perfusion. In order to avoid the effect of rundown of the channel current on the experimental results, the experiment was completed within 20 min after cell membrane breaking (Dan et al, 2015;Zhang et al, 2015). The sampled data were stored for measurement and analysis of the electrophysiological characteristics of the channel.…”

Section: Electrophysiological Recordingsmentioning

confidence: 99%

Effects of Allicin on Late Sodium Current Caused by ΔKPQ-SCN5A Mutation in HEK293 Cells

et al. 2021

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AimThe aim was to study the effect of Allitridum (Allicin) on the heterologous expression of the late sodium current on the ΔKPQ-SCN5A mutations in HEK293 cells, with a view to screening new drugs for the treatment of long QT syndrome type 3 (LQT3).Methods and ResultsThe ΔKPQ-SCN5A plasmid was transiently transferred into HEK293 cells by liposome technology and administered by extracellular perfusion, and the sodium current was recorded by whole-cell patch-clamp technology. Application of Allicin 30 μM reduced the late sodium current (INa,L) of the Nav1.5 channel current encoded by ΔKPQ-SCN5A from 1.92 ± 0.12 to 0.65 ± 0.03 pA/pF (P < 0.01, n = 15), which resulted in the decrease of INa,L/INa,P (from 0.94% ± 0.04% to 0.32% ± 0.02%). Furthermore, treatment with Allicin could move the steady-state inactivation of the channel to a more negative direction, resulting in an increase in channel inactivation at the same voltage, which reduced the increase in the window current and further increased the inactivation of the channel intermediate state. However, it had no effect on channel steady-state activation (SSA), inactivation mechanics, and recovery dynamics after inactivation. What’s more, the Nav1.5 channel protein levels of membrane in the ΔKPQ-SCN5A mutation were enhanced from 0.49% ± 0.04% to 0.76% ± 0.02% with the effect of 30 mM Allicin, close to 0.89% ± 0.02% of the WT.ConclusionAllicin reduced the late sodium current of ΔKPQ-SCN5A, whose mechanism may be related to the increase of channel steady-state inactivation (SSI) and intermediate-state inactivation (ISI) by the drug, thus reducing the window current.

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Section: Electrophysiological Recordingsmentioning

confidence: 99%