<> "The repository administrator has not yet configured an RDF license."^^ . <> . . "Intravenous anaesthetics inhibit nicotinic receptor-induced membrane currents and Ca 2+ -transients in rat intracardiac neurons"^^ . "The effects of intravenous (i.v.) anaesthetics on nicotinic acetylcholine receptor (nAChR)-mediated transients in intracellular free Ca2+ concentration ([Ca2+]i) and currents were investigated in neonatal rat intracardiac neurons using fura-2 photometry and patch-clamp recordings. Extensive preliminary tests using fura-2 containing solutions in the presence or absence of the anaesthetics were carried out to detect any interference of these drugs with the fura-2 fluorescence signal: Using photospectrometry and a ratiometric photometry set-up to carry out a series of calibrations of the fura-2 signal revealed that ratiometric fura-2 recordings can faithfully be carried out in the presence of clinically relevant concentrations (clinical EC50) of the i.v. anaesthetics studied. In fura-2 loaded neurons, nAChR activation evoked a transient increase in [Ca2+]i, which was reversibly inhibited by the clinical EC50 of the i.v. anaesthetic thiopental. The EC50 for thiopental inhibition of nAChR induced [Ca2+]i transients was 28 µM, close to the estimated clinical EC50 of thiopental (25 µM). However, control experiments using Ca2+ -channel blockers showed that voltage-gated Ca2+ -channels (Cav) are activated by the depolarization following nAChR activation and thus indirectly contribute to increases in [Ca2+]i. When fura-2 loaded neurons were voltage-clamped at -60 mV to eliminate any contribution of voltage-gated Ca2+ channels, then thiopental simultaneously inhibited nAChR-induced increases in [Ca2+]i and peak current amplitudes. Thiopental inhibited nAChR-induced peak current amplitudes in dialyzed whole cell recordings by ~ 40 % at -120, -80 and -40 mV holding potential suggesting that the inhibition is voltage independent. Thiopental did not inhibit caffeine-induced [Ca2+]i transients, indicating that an inhibition of Ca2+ release from internal stores via ryanodine receptor (RyR) channels is unlikely. The barbiturate pentobarbital and the dissociative anaesthetic ketamine used at clinical EC50 concentrations were also shown to inhibit nAChR-induced increases in [Ca2+]i. In conclusion, thiopental and other i.v. anaesthetics may inhibit nAChR-induced currents and [Ca2+]i transients in intracardiac neurons by binding to nAChR and thereby may contribute to changes in heart rate and cardiac output under clinical conditions."^^ . "2003" . . . . . . . . "Martin"^^ . "Weber"^^ . "Martin Weber"^^ . . . . . . "Intravenous anaesthetics inhibit nicotinic receptor-induced membrane currents and Ca 2+ -transients in rat intracardiac neurons (PDF)"^^ . . . "mweber_diss2003.pdf"^^ . . . "Intravenous anaesthetics inhibit nicotinic receptor-induced membrane currents and Ca 2+ -transients in rat intracardiac neurons (Other)"^^ . . . . . . "small.jpg"^^ . . . "Intravenous anaesthetics inhibit nicotinic receptor-induced membrane currents and Ca 2+ -transients in rat intracardiac neurons (Other)"^^ . . . . . . "medium.jpg"^^ . . . "Intravenous anaesthetics inhibit nicotinic receptor-induced membrane currents and Ca 2+ -transients in rat intracardiac neurons (Other)"^^ . . . . . . "preview.jpg"^^ . . . "Intravenous anaesthetics inhibit nicotinic receptor-induced membrane currents and Ca 2+ -transients in rat intracardiac neurons (Other)"^^ . . . . . . "lightbox.jpg"^^ . . "HTML Summary of #4312 \n\nIntravenous anaesthetics inhibit nicotinic receptor-induced membrane currents and Ca 2+ -transients in rat intracardiac neurons\n\n" . "text/html" . . . "570 Biowissenschaften, Biologie"@de . "570 Life sciences"@en . .