{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T17:05:44Z","timestamp":1777482344033,"version":"3.51.4"},"reference-count":38,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2009,1,29]],"date-time":"2009-01-29T00:00:00Z","timestamp":1233187200000},"content-version":"vor","delay-in-days":303,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2008,4]]},"abstract":"<jats:sec><jats:title>Background and purpose:<\/jats:title><jats:p>TRPC5 is a mammalian homologue of the <jats:italic>Drosophila<\/jats:italic> Transient Receptor Potential (TRP) channel and has expression and functions in the cardiovascular and nervous systems. It forms a calcium\u2010permeable cation channel that can be activated by a variety of signals including carbachol (acting at muscarinic receptors), lanthanides (e.g. Gd<jats:sup>3+<\/jats:sup>) and phospholipids (e.g. lysophosphatidylcholine: LPC). Here we report the effects of inhalational (halothane and chloroform) and intravenous (propofol) general anaesthetics upon TRPC5.<\/jats:p><\/jats:sec><jats:sec><jats:title>Experimental approach:<\/jats:title><jats:p>Human TRPC5 channels were expressed in HEK 293 cells and studied using fura\u20102 and patch\u2010clamp recording to measure intracellular calcium and membrane currents respectively at room temperature. Human TRPM2 channels were studied for comparison.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key results:<\/jats:title><jats:p>TRPC5 activation by carbachol, Gd<jats:sup>3+<\/jats:sup> or LPC was inhibited by halothane and chloroform at 0.1 and 0.2\u2003m<jats:sc>M<\/jats:sc> respectively. Neither agent inhibited TRPM2. Propofol had an initial stimulatory effect on TRPC5 (evident in patch\u2010clamp recordings only) and an inhibitory effect at 10\u2003\u03bc<jats:sc>M<\/jats:sc>. TRPM2 was not affected by propofol. Propofol inhibited activation of TRPC5 by Gd<jats:sup>3+<\/jats:sup> but not LPC, suggesting the effect was not directly on the channel. Propofol's anti\u2010oxidant property was not necessary for its inhibitory effect because di\u2010isopropyl benzene, a propofol analogue that lacks the hydroxyl group, also inhibited TRPC5.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions and implications:<\/jats:title><jats:p>The data show the sensitivity of TRPC5 channel to general anaesthetics and suggest that some of the effects could have clinical relevance. The effects may be explained in part by the sensitivity of the channel to biophysical properties of the lipid bilayer.<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (2008) <jats:bold>153<\/jats:bold>, 1505\u20131512; doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/sj.bjp.0707689\">10.1038\/sj.bjp.0707689<\/jats:ext-link>; published online 21 January 2008<\/jats:p><\/jats:sec>","DOI":"10.1038\/sj.bjp.0707689","type":"journal-article","created":{"date-parts":[[2008,1,21]],"date-time":"2008-01-21T13:23:52Z","timestamp":1200921832000},"page":"1505-1512","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["Modulation of TRPC5 cation channels by halothane, chloroform and propofol"],"prefix":"10.1111","volume":"153","author":[{"given":"Y 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