{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T19:11:59Z","timestamp":1792177919533,"version":"4.4.0"},"reference-count":43,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2009,1,29]],"date-time":"2009-01-29T00:00:00Z","timestamp":1233187200000},"content-version":"vor","delay-in-days":1489,"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":[[2005,1]]},"abstract":"<jats:p>\n<jats:list list-type=\"explicit-label\">\n<jats:list-item><jats:p>The effects of intravenous (i.v.) anaesthetics on nicotinic acetylcholine receptor (nAChR)\u2010induced transients in intracellular free Ca<jats:sup>2+<\/jats:sup> concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) and membrane currents were investigated in neonatal rat intracardiac neurons.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>In fura\u20102\u2010loaded neurons, nAChR activation evoked a transient increase in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>I<\/jats:sub>, which was inhibited reversibly and selectively by clinically relevant concentrations of thiopental. The half\u2010maximal concentration for thiopental inhibition of nAChR\u2010induced [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> transients was 28\u2003<jats:italic>\u03bc<\/jats:italic><jats:sc>M<\/jats:sc>, close to the estimated clinical EC<jats:sub>50<\/jats:sub> (clinically relevant (half\u2010maximal) effective concentration) of thiopental.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>In fura\u20102\u2010loaded neurons, voltage clamped at \u221260\u2003mV to eliminate any contribution of voltage\u2010gated Ca<jats:sup>2+<\/jats:sup> channels, thiopental (25\u2003<jats:italic>\u03bc<\/jats:italic><jats:sc>M<\/jats:sc>) simultaneously inhibited nAChR\u2010induced increases in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> and peak current amplitudes. Thiopental inhibited nAChR\u2010induced peak current amplitudes in dialysed whole\u2010cell recordings by \u223c 40% at \u2212120, \u221280 and \u221240\u2003mV holding potential, indicating that the inhibition is voltage independent.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>The barbiturate, pentobarbital and the dissociative anaesthetic, ketamine, used at clinical EC<jats:sub>50<\/jats:sub> were also shown to inhibit nAChR\u2010induced increases in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> by \u223c40%.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Thiopental (25\u2003<jats:italic>\u03bc<\/jats:italic><jats:sc>M<\/jats:sc>) did not inhibit caffeine\u2010, muscarine\u2010 or ATP\u2010evoked increases in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>, indicating that inhibition of Ca<jats:sup>2+<\/jats:sup> release from internal stores <jats:italic>via<\/jats:italic> either ryanodine receptor or inositol\u20101,4,5\u2010trisphosphate receptor channels is unlikely.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Depolarization\u2010activated Ca<jats:sup>2+<\/jats:sup> channel currents were unaffected in the presence of thiopental (25\u2003<jats:italic>\u03bc<\/jats:italic><jats:sc>M<\/jats:sc>), pentobarbital (50\u2003<jats:italic>\u03bc<\/jats:italic><jats:sc>M<\/jats:sc>) and ketamine (10\u2003<jats:italic>\u03bc<\/jats:italic><jats:sc>M<\/jats:sc>).<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>In conclusion, i.v. anaesthetics inhibit nAChR\u2010induced currents and [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> transients in intracardiac neurons by binding to nAChRs and thereby may contribute to changes in heart rate and cardiac output under clinical conditions.<\/jats:p><\/jats:list-item>\n<\/jats:list>\n<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (2005) <jats:bold>144<\/jats:bold>, 98\u2013107. doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/sj.bjp.0705942\">10.1038\/sj.bjp.0705942<\/jats:ext-link><\/jats:p>","DOI":"10.1038\/sj.bjp.0705942","type":"journal-article","created":{"date-parts":[[2005,1,11]],"date-time":"2005-01-11T19:56:48Z","timestamp":1105473408000},"page":"98-107","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":31,"title":["Intravenous anaesthetics inhibit nicotinic acetylcholine receptor\u2010mediated currents and Ca<sup>2+<\/sup> transients in rat intracardiac ganglion 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