Ethanol potentiation of 5-HT3 receptor-mediated ion current in NCB-20 neuroblastoma cells

doi:10.1016/0304-3940(91)90192-V

Neuroscience Letters

Volume 122, Issue 1, 14 January 1991, Pages 57-60

https://doi.org/10.1016/0304-3940(91)90192-V Get rights and content

Abstract

The effect of acute ethanol (EtOH) exposure on 5-HT₃ receptor-mediated ion current was examined in whole-cell patch-clamp recordings from NCB-20 neuroblastoma cells. The physiologic and pharmacologic properties of 5-HT-activated ion current in NCB-20 cells indicated that it was mediated by 5-HT₃ receptors. EtOH potentiated 5-HT₃ receptor-mediated current in a concentration-dependent manner at concentrations (25–100 mM) which are achieved during EtOH intoxication in vivo.

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Ethanol potentiation of 5-HT3 receptor-mediated ion current in NCB-20 neuroblastoma cells

Abstract

Eur. J. Pharmacol.

Pharmacol. Biochem. Behav.

Trends Pharmacol. Sci.

Prog. Neuropsychopharmacol. Biol. Psychiatry

Neuron

Serotonin receptor-mediated activation of adenylate cyclase in the neuroblastoma NCB.20: A novel 5-hydroxytryptamine receptor

Mol. Pharmacol.

5-HT3 receptors are membrane ion channels

Nature

Blockade of the discriminative stimulus properties of ethanol by antagonists of the 5-HT3 receptor

FASEB J.

Ethanol, anaesthetics and other lipophilic drugs preferentially inhibit 5-hydroxytryptamine- and acetylcholine-induced noradrenaline release from sympathetic nerves

Arch. Int. Pharmacodyn. Ther.

N-methyl-d-aspartate receptors and ethanol: inhibition of calcium flux and cyclic GMP production

J. Neurochem.

Ethanol potentiation of 5-HT₃ receptor-mediated ion current in NCB-20 neuroblastoma cells

5-HT₃ receptors are membrane ion channels

Blockade of the discriminative stimulus properties of ethanol by antagonists of the 5-HT₃ receptor

$N- methyl- d -aspartate$ receptors and ethanol: inhibition of calcium flux and cyclic GMP production