On the interaction between BDNF and serotonin systems: The effects of long-term ethanol consumption in mice

Попова, Н. К.; Ilchibaeva, Tatiana V.; Antonov, E. V.; Pershina, A.; Базовкина, Д. В.; Науменко, В. С.

doi:10.1016/j.alcohol.2020.04.002

Cited by 27 publications

(17 citation statements)

References 89 publications

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“…The effects of chronic voluntary ethanol consumption on neuroadaptations within the 5-HT neurotransmission, particularly in the raphe nuclei, have been studied to a limited extent. Consistent with our findings, a recent study has demonstrated no change in Tph2 mRNA level in the raphe nuclei of mice after chronic (for 6 weeks) 10% ethanol consumption [ 85 ]. Additionally, Popova et al [ 85 ] have shown increases in the activity of the TPH2 enzyme and 5-HT turnover, and the transcript level (but not protein) of the 5-HT 7 receptor in the midbrain raphe nuclei of animals after chronic ethanol intake.…”

Section: Discussionsupporting

confidence: 93%

“…Consistent with our findings, a recent study has demonstrated no change in Tph2 mRNA level in the raphe nuclei of mice after chronic (for 6 weeks) 10% ethanol consumption [ 85 ]. Additionally, Popova et al [ 85 ] have shown increases in the activity of the TPH2 enzyme and 5-HT turnover, and the transcript level (but not protein) of the 5-HT 7 receptor in the midbrain raphe nuclei of animals after chronic ethanol intake. Importantly, no change in 5-HT content and 5-HT 1A receptor gene expression has been reported in the midbrain, frontal cortex, hippocampus, hypothalamus, and amygdala of mice after chronic ethanol [ 85 ].…”

Section: Discussionsupporting

confidence: 93%

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Tph2 Gene Expression Defines Ethanol Drinking Behavior in Mice

Zaniewska

Mosienko

Bäder

et al. 2022

Cells

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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.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 93%

Tph2 Gene Expression Defines Ethanol Drinking Behavior in Mice

Zaniewska

Mosienko

Bäder

et al. 2022

Cells

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“…As ethanol exposure activates the hypothalamic-pituitary-adrenal axis acting as a physiological stressor, it has been hypothesized that PPAC impacts stress responsivity of offspring [122,123]. This hypothesis seems to be partially confirmed as the studies show ethanol-sired male offspring sexspecific blunted plasma corticosterone levels in response to acute restraint stress, resistance to stressinduced excessive fluid intake, enhanced sensitivity to the anxiolytic and motor-enhancing effects of ethanol, reduced ethanol preference and consumption, altered BDNF (brain-derived neurotrophic factor) and/or NGF (nerve growth factor) (well-known regulators of ethanol drinking behavior [16,26,117,[124][125][126][127][128][129][130][131][132][133][134][135][136][137][138][139][140][141][142]) expression in the ventral tegmental area compared to control-sired male offspring. No differences among ethanol-and control-sired female offspring have been found on these assays.…”

Section: Emotional Responsementioning

confidence: 99%

Transgenerational Abnormalities Induced by Paternal Preconceptual Alcohol Drinking: Findings from Humans and Animal Models

Terracina

Ferraguti

Tarani

et al. 2022

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: Alcohol consumption during pregnancy and lactation is a widespread preventable cause of neurodevelopmental impairment in newborns. While the harmful effects of gestational alcohol use have been well documented, only recently the role of paternal preconceptual alcohol consumption (PPAC) prior to copulating has drawn specific epigenetic considerations. Solid human and animal model data demonstrated that PPAC may affect sperm function eliciting oxidative stress. In newborns, PPAC may induce changes in the behavior, cognitive functions and emotional responses. Furthermore, PPAC may elicit neurobiological disruptions, visuospatial impairments, hyperactivity disorders, motor skill disruptions, hearing loss, endocrine and immune alterations, reduced physical growth, placental disruptions and metabolic alterations. Neurobiological studies on PPAC disclosed also changes in brain function and structure by the disruption of the growth factors pathways. In particular, as shown in animal model studies PPAC alters brain nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) synthesis and release. This review shows that the crucial topic of lifelong disabilities induced by PPAC and/or gestational alcohol drinking is quite challenging at the individual, societal, and familial levels. Since a nontoxic drinking behavior before pregnancy (for both men and women) during pregnancy and lactation cannot be established the only suggestion for couples planning pregnancies is to completely avoid the consumption of alcoholic beverages.

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“…Similarly, mixed findings were also reported for 5-HT1A and 5-HT2A receptor bindings (Underwood et al, 2008 , 2018 ; Storvik et al, 2009 ). Chronic alcohol intake increases the metabolites of serotonin in the raphe nuclei area, however reduces 5-HT2A protein levels in the mice cortex, indicating reduced serotonergic activity (Popova et al, 2020 ). Acute alcohol intake reduces tryptophan availability to the brain (non-aggressive), which leads to a decrease in serotonin synthesis and turnover, about 25% of the concentration of tryptophan following an oral intake of alcohol (Badawy et al, 1995 ).…”

Section: Serotonin In Aud and Aggressionmentioning

confidence: 99%

Alcohol, Aggression, and Violence: From Public Health to Neuroscience

et al. 2021

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Alcohol has been associated with violent crimes and domestic violence across many nations. Various etiological factors were linked to chronic alcohol use and violence including psychiatric comorbidities of perpetrators such as personality disorders, mood disorders, and intermittent explosive disorders. Aggression is the precursor of violence and individuals prone to aggressive behaviors are more likely to commit impulsive violent crimes, especially under the influence of alcohol. Findings from brain studies indicate long-term alcohol consumption induced morphological changes in brain regions involved in self-control, decision-making, and emotional processing. In line with this, the inherent dopaminergic and serotonergic anomalies seen in aggressive individuals increase their susceptibility to commit violent crimes when alcohol present in their system. In relation to this, this article intends to investigate the influence of alcohol on aggression with sociopsychological and neuroscientific perspectives by looking into comorbidity of personality or mood disorders, state of the mind during alcohol consumption, types of beverages, environmental trigger, neurochemical changes, and gender differences that influence individual responses to alcohol intake and susceptibility to intoxicated aggression.

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On the interaction between BDNF and serotonin systems: The effects of long-term ethanol consumption in mice

Cited by 27 publications

References 89 publications

Tph2 Gene Expression Defines Ethanol Drinking Behavior in Mice

Tph2 Gene Expression Defines Ethanol Drinking Behavior in Mice

Transgenerational Abnormalities Induced by Paternal Preconceptual Alcohol Drinking: Findings from Humans and Animal Models

Alcohol, Aggression, and Violence: From Public Health to Neuroscience

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