IndraLab

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"In mammals, diethyl ether and chloroform are known to activate TREK-1, a two-pore-domain potassium (K2P) channel ."

"Tissue studies have been performed on these K + channels. xref examined TASK and TREK-1, and found that TREK-1 was activated by chloroform, diethyl ether, halothane and isoflurane, while TASK was activated by halothane and isoflurane. xref engineered human TRESK channels into the Xenopus oocyte, and noted that their outward currents were potentiated 1.5- to 3-fold by different haloalkane GAs. xref expressed TREK-1 channels on HEK-293 cells and showed that TREK-1 currents were enhanced by nitrous oxide, xenon, cyclopropane and halothane. xref cloned a TASK channel from the mollusc Lymnaea stagnalis and discovered that it was preferentially activated by (+)-isoflurane; this was also observed in mice ( xref and rats ( xref ."

"Inhaled anesthetics xenon , diethyl ether , halothane , and chloroform robustly activate TREK-1 at concentrations relevant to their clinical use ( 30 , 31 ) ."

"isoflurane, chloroform, diethyl ether) activate TREK-1 and genetic deletion of TREK-1 decreases anesthesia sensitivity in mice [2–4]."

"(A) Representative TREK-1 whole-cell currents activated by chloroform (1 mM) in physiological K+ gradients."

"Inhaled anesthetics xenon, diethyl ether, halothane, and chloroform robustly activate TREK-1 at concentrations relevant to their clinical use (30, 31) ."