Ethanol potentiation of 5-HT3 receptor-mediated ion current in NCB-20 neuroblastoma cells
References (20)
- et al.
Differential inhibitory effects of a 5-HT3 antagonist on drug-induced stimulation of dopamine release
Eur. J. Pharmacol.
(1989) - et al.
Regional levels of monoamines in alcohol-preferring and non-preferring lines of rats
Pharmacol. Biochem. Behav.
(1982) - et al.
Electrophysiology of 5-HT3 receptors in neuronal cell lines
Trends Pharmacol. Sci.
(1989) - et al.
Reduced central serotonin turnover in a subgroup of alcoholics
Prog. Neuropsychopharmacol. Biol. Psychiatry
(1987) - et al.
5-HT3 receptors mediate rapid responses in cultured hippocampus and a clonal cell line
Neuron
(1988) - et al.
Serotonin receptor-mediated activation of adenylate cyclase in the neuroblastoma NCB.20: A novel 5-hydroxytryptamine receptor
Mol. Pharmacol.
(1990) - et al.
5-HT3 receptors are membrane ion channels
Nature
(1989) - et al.
Blockade of the discriminative stimulus properties of ethanol by antagonists of the 5-HT3 receptor
FASEB J.
(1990) - et al.
Ethanol, anaesthetics and other lipophilic drugs preferentially inhibit 5-hydroxytryptamine- and acetylcholine-induced noradrenaline release from sympathetic nerves
Arch. Int. Pharmacodyn. Ther.
(1979) - et al.
receptors and ethanol: inhibition of calcium flux and cyclic GMP production
J. Neurochem.
(1989)
Cited by (96)
Ethanol's Action Mechanisms in the Brain: From Lipid General Alterations to Specific Protein Receptor Binding
2017, Addictive Substances and Neurological Disease: Alcohol, Tobacco, Caffeine, and Drugs of Abuse in Everyday LifestylesMolecular basis of alcoholism
2014, Handbook of Clinical NeurologyCitation Excerpt :Increased serotonergic transmission is associated with less alcohol consumption and less serotonergic transmission is linked to more alcohol consumption, in animal models of drinking and in human alcoholics (for review, see Lovinger, 1997). Electrophysiologic recordings in neuroblastoma cells show that acute alcohol potentiates 5-HT3 receptor-mediated ion currents (Lovinger, 1991). Acute alcohol was also found to activate the 5-HT3 receptor in oocytes (Harris et al., 1995), ganglion neurons (Lovinger and White, 1991), frontal cortex neurons (Sung et al., 2000), and human embryonic kidney 293 cells (Lovinger and Zhou, 1994).
Ethanol Action on Dopaminergic Neurons in the Ventral Tegmental Area. Interaction with Intrinsic Ion Channels and Neurotransmitter Inputs
2010, International Review of NeurobiologyCitation Excerpt :Meanwhile, ethanol (2 g/kg, i.p.) stimulated DA release in the VTA by only ∼50% over baseline levels, and, most importantly, this stimulatory action of ethanol on somatodendritic DA release was completely blocked by the 5-HT3 antagonist. These findings indicate that the potentiating effect of ethanol on 5-HT3 receptor function within the VTA may be critically involved in the activation of mesolimbic DA circuits (Lovinger, 1991). In support of this idea, it has been shown that both the acquisition and maintenance of intra-VTA self-administration of ethanol can be completely prevented by co-administration of a 5-HT3 antagonist (Rodd et al., 2005c; Rodd-Henricks et al., 2003).
Distinct molecular basis for differential sensitivity of the serotonin type 3A receptor to ethanol in the absence and presence of agonist
2002, Journal of Biological Chemistry