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Tph2 gene expression defines ethanol drinking behavior in mice

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Item Type:Article
Title:Tph2 gene expression defines ethanol drinking behavior in mice
Creators Name:Zaniewska, M. and Mosienko, V. and Bader, M. and Alenina, N.
Abstract:Indirect evidence supports a link between disrupted serotonin (5-hydroxytryptamine; 5-HT) signaling in the brain and addictive behaviors. However, the effects of hyposerotonergia on ethanol drinking behavior are contradictory. In this study, mice deficient in tryptophan hydroxylase 2 (Tph2(-/-)), the rate-limiting enzyme of 5-HT synthesis in the brain, were used to assess the role of central 5-HT in alcohol drinking behavior. Life-long 5-HT depletion in these mice led to an increased ethanol consumption in comparison to wild-type animals in a two-bottle choice test. Water consumption was increased in naïve 5-HT-depleted mice. However, exposure of Tph2(-/-) animals to ethanol resulted in the normalization of water intake to the level of wild-type mice. Tph2 deficiency in mice did not interfere with ethanol-evoked antidepressant response in the forced swim test. Gene expression analysis in wild-type animals revealed no change in Tph2 expression in the brain of mice consuming ethanol compared to control mice drinking water. However, within the alcohol-drinking group, inter-individual differences in chronic ethanol intake correlated with Tph2 transcript levels. Taken together, central 5-HT is an important modulator of drinking behavior in mice but is not required for the antidepressant effects of ethanol.
Keywords:Central 5-HT, Ethanol, Raphe Nuclei, Tph2 Knockout, Tph2 Transcript, Animals, Mice
Page Range:874
Date:3 March 2022
Official Publication:https://doi.org/10.3390/cells11050874
PubMed:View item in PubMed

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