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Characterization of an eag‐like potassium channel in human neuroblastoma cells
Author(s) -
Meyer Roman,
Heinemann Stefan H.
Publication year - 1998
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1998.049br.x
Subject(s) - herg , depolarization , intracellular , chemistry , biophysics , patch clamp , retinoic acid , potassium channel , extracellular , microbiology and biotechnology , biochemistry , biology , receptor , gene
1 SH‐SY5Y human neuroblastoma cells were investigated with whole‐cell and perforated patch recording methods. 2 Besides a quickly activating delayed rectifier channel and a HERG‐like channel, a slowly activating potassium channel with biophysical properties identical to those of rat eag (r‐eag) channels was detected, here referred to as h‐eag. 3 h‐eag shows a marked Cole‐Moore shift, i.e. the activation kinetics become very slow when the depolarization starts from a very negative holding potential. In addition, extracellular Mg 2+ and Ni 2+ strongly slow down activation. 4 Application of acetylcholine induces a fast block of the current when recorded in the perforated patch mode. This block is presumably mediated by Ca 2+ , as about 1 μM intracellular Ca 2+ completely abolished h‐eag outward current. 5 When cells were grown in the presence of 10 μM retinoic acid in order to synchronize the cell line in the G1 phase of the cell cycle, h‐eag current was reduced to less than 5 % of the control value, while the delayed rectifier channel was expressed more abundantly. Down‐regulation of h‐eag by long‐term exposure to retinoic acid was paralleled by a right shift in the activation potential of HERG‐like channels. 6 Acute application of 10 μM retinoic acid blocked the delayed rectifier channel but enhanced the h‐eag current. 7 Thus, our results show that human neuroblastoma cells express in a cell cycle‐dependent manner an [Mg 2+ ] o ‐dependent potassium channel (h‐eag) which is blocked by submicromolar concentrations of intracellular Ca 2+ .