Effects of propofol and thiopentone on potassium- and carbachol-evoked [3H]noradrenaline release and increased [Ca2+]i from SH-SY5Y human neuroblastoma cells
Abstract We have examined the effects of two intravenous anaesthetic induction agents, propofol and thiopentone, on K + and carbachol evoked [ 3 H]noradrenaline release from a human neuroblastoma cell line, SH-SY5Y. In this model, we have previously demonstrated that K + evoked [ 3 H]noradrenaline release was dependent on Ca 2+ entry and carbachol evoked release was extracellular Ca 2+ -independent. Propofol inhibited K + (100 mM)-evoked ( IC 50 of 42 ± 11 μM), but not carbachol (1 mM)-evoked, [ 3 H]noradrenaline release. Thiopentone inhibited both K + - and carbachol-evoked release with IC 50 values of 116 ± 15 μM and 169 ± 39 μM, respectively. These inhibitory effects were not due to changes in the release dynamics, as assessed using perfused cells. Furthermore, thiopentone inhibition of carbachol-evoked release was not due to muscarinic receptor antagonism. Both propofol and thiopentone caused noncompetitive inhibition of K + -stimulated Ca 2+ influx, with IC 50 values of 127 ± 7 μM and 121 ± 10 μM, respectively. These effects were not due to interaction with GABA A receptors, but suggest that both compounds block voltage-sensitive Ca 2+ channels. Thiopentone, but not propofol, inhibited carbachol-stimulated increased intracellular Ca 2+ concentrations in the presence and absence of extracellular Ca 2+ . However, thiopentone had no effect on carbachol-stimulated inositol (1,4,5)-triphosphate formation, suggesting that thiopentone may directly inhibit Ca 2+ release from intracellular stores.
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