Modulation of TRPC5 cation channels by halothane, chloroform and propofol.

British Journal of Pharmacology
Yahya M BahnasiDavid J Beech

Abstract

TRPC5 is a mammalian homologue of the Drosophila Transient Receptor Potential (TRP) channel and has expression and functions in the cardiovascular and nervous systems. It forms a calcium-permeable cation channel that can be activated by a variety of signals including carbachol (acting at muscarinic receptors), lanthanides (e.g. Gd3+) and phospholipids (e.g. lysophosphatidylcholine: LPC). Here we report the effects of inhalational (halothane and chloroform) and intravenous (propofol) general anaesthetics upon TRPC5. Human TRPC5 channels were expressed in HEK 293 cells and studied using fura-2 and patch-clamp recording to measure intracellular calcium and membrane currents respectively at room temperature. Human TRPM2 channels were studied for comparison. TRPC5 activation by carbachol, Gd3+ or LPC was inhibited by halothane and chloroform at > or =0.1 and 0.2 mM respectively. Neither agent inhibited TRPM2. Propofol had an initial stimulatory effect on TRPC5 (evident in patch-clamp recordings only) and an inhibitory effect at > or =10 microM. TRPM2 was not affected by propofol. Propofol inhibited activation of TRPC5 by Gd3+ but not LPC, suggesting the effect was not directly on the channel. Propofol's anti-oxidant property was not...Continue Reading

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Mar 17, 2010·British Journal of Anaesthesia·P M Hopkins
Jun 9, 2009·Pharmacology & Therapeutics·Ryuji InoueYasuhiro Kawarabayashi
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May 29, 2020·Neuropharmacology·Matjaž StenovecRobert Zorec
Mar 28, 2009·Cell Calcium·David J BeechEman Al-Shawaf

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