Ethanol-induced epigenetic regulations at the Bdnf gene in C57BL/6J mice

Stragier, E.; Massart, Renaud; Salery, Marine; Hamon, Michel; Geny, David; Martin, Valérie; Boulle, Fabien; Lanfumey, Laurence

doi:10.1038/mp.2014.38

Cited by 53 publications

(54 citation statements)

References 45 publications

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“…Moderate, chronic ethanol consumption has been observed to induce epigenetic changes in the hippocampus of mice (Stragier et al, 2015). Particularly, epigenetic modifications to the Bdnf gene correlate with increased BDNF expression and subsequent stimulation of neurogenesis in the subgranular zone of the dentate gyrus through TrkB receptor activation.…”

Section: Gdnf and Bdnf In Drug Seeking Behavior In Laboratory Animalsmentioning

confidence: 99%

Update of neurotrophic factors in neurobiology of addiction and future directions

Koskela

Bäck

Võikar

et al. 2017

Neurobiology of Disease

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Drug addiction is a chronic brain disease and drugs of abuse cause long lasting neuroadaptations. Addiction is characterized by the loss of control over drug use despite harmful consequences, and high rates of relapse even after long periods of abstinence. Neurotrophic factors (NTFs) are well known for their actions on neuronal survival in the peripheral nervous system. Moreover, NTFs have been shown to be involved in synaptic plasticity in the brain. Brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) are two of the most studied NTFs and both of them have been reported to increase craving when administered into the mesocorticolimbic dopaminergic system after drug self-administration. Here we review recent data on BDNF and GDNF functions in addiction-related behavior and discuss them in relation to previous findings. Finally, we give an insight into how new technologies could aid in further elucidating the role of these factors in drug addiction.

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Section: Gdnf and Bdnf In Drug Seeking Behavior In Laboratory Animalsmentioning

confidence: 99%

Update of neurotrophic factors in neurobiology of addiction and future directions

Koskela

Bäck

Võikar

et al. 2017

Neurobiology of Disease

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“…Stragier et al reported that chronic and moderate EtOH intake produces marked epigenetic changes that result in the overexpression of brainderived neurotrophic factor (BDNF) and downstream hippocampal neurogenesis in C57BL/6J mice (72). In contrast, Ebada et al reported that C57BL/6J mice suffered from memory deficit due to a chronic intermittent intake of a low dose (1% EtOH) of ethanol (73).…”

Section: Ort and Oltmentioning

confidence: 99%

Moderate-dose Regular Lifelong Alcohol Intake Changes the Intestinal Flora, Protects against Aging, and Keeps Spatial Memory in the Senescence-accelerated Mouse Prone 8 (SAMP8) Model

et al. 2016

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-Purpose: Heavy and long-term alcohol consumption increase the risk of alcohol-related diseases. Epidemiological studies show moderate drinking reduces the risk of mortality, cardiovascular diseases, and brain infarction in the J-shaped or U-shaped curve effect. However, why moderate drinkers may be healthy and non-drinkers may be ill in diverse populations remains controversial. Herein, we examined the relationship between moderate/lifelong alcohol intake and aging, especially aging-related cognitive functions in senescenceaccelerated mouse prone 8 (SAMP8) model. Methods: SAMP8 model (5-week-old, male, n = 36), a model of age-related cognitive deficit, were group-housed (n = 6/cage) and provided free access to water (water group, n = 18) or 1% ethanol (EtOH group, n = 18, intake started when mice were 9 weeks old). The object recognition test (ORT) and object location test (OLT) were used to evaluate cognitive functions. The intestinal flora at the age of 87 weeks was analyzed by terminal restriction fragment length polymorphism (T-RFLP). Results: The lifespan of the EtOH-group mice was about 4 weeks longer than that of the water-group mice. In the EtOH group, spatial recognition impairment, assessed by OLT, was observed later (age, 73 weeks) than that in the water group (age, 52 weeks). The spinal curvature and skin conditions progressed significantly slower in the EtOH group than in the water group. Moreover, diarrhea symptoms only appeared in the water group, at the age of 82 weeks. The T-RFLP analysis of the intestinal flora indicated higher Lactobacillales order and lower Clostridium cluster XI in the EtOH group than in the water group, although those were extremely high in some mice close to death in both groups. Water-group mice with diarrhea presented significantly higher Clostridium cluster XI than did those without diarrhea (P = 0.017). Conclusion: Moderate alcohol intake changes intestinal flora and positively affects aging of SAMP8 model.This article is open to POST-PUBLICATION REVIEW. Registered readers (see "For Readers") may comment by clicking on ABSTRACT on the issue's contents page.

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“…In the rat amygdala, acute ethanol increases global and prodynorphin and pronociceptin promoter histone acetylation levels (Pandey et al, 2008; D’Addario et al, 2013), and reduces prodynophin and pronociceptin H3K27me3 binding (D’Addario et al, 2013). Moreover, in the hippocampus, ethanol-induced histone H3 acetylation and H3K4me3 have been found to regulate expression of brain derived neurotrophic factor (BDNF) exons (Stragier et al, 2015). Finally, acute ethanol withdrawal leads to decreased histone acetylation in the rat amygdala (Pandey et al, 2008; Sakharkar et al, 2012; Moonat et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Stable Histone Methylation Changes at Proteoglycan Network Genes Following Ethanol Exposure

et al. 2018

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Alcohol use disorder (AUD) is a chronic mental illness in which patients often achieve protracted periods of abstinence prior to relapse. Epigenetic mechanisms may provide an explanation for the persisting gene expression changes that can be observed even after long periods of abstinence and may contribute to relapse. In this study, we examined two histone modifications, histone 3 lysine 4 tri-methylation (H3K4me3) and histone 3 lysine 27 tri-methylation (H3K27me3), in the prefrontal cortex of Withdrawal Seizure Resistant (WSR) mice 21 days after 72 h of ethanol vapor exposure. These histone modifications were selected because they are associated with active promoters (H3K4me3) and repressed gene expression in a euchromatic environment (H3K27me3). We performed a genome-wide analysis to identify differences in H3K4me3 and H3K27me3 levels in post-ethanol exposure vs. control mice by ChIP-seq. We detected a global reduction in H3K4me3 peaks and increase in H3K27me3 peaks in post-ethanol exposure mice compared to controls, these changes are consistent with persistent reductions in gene expression. Pathway analysis of genes displaying changes in H3K4me3 and H3K27me3 revealed enrichment for genes involved in proteoglycan and calcium signaling pathways, respectively. Microarray analysis of 7,683 genes and qPCR analysis identified eight genes displaying concordant regulation of gene expression and H3K4me3/H3K27me3. We also compared changes in H3K4me3 and/or H3K27me3 from our study with changes in gene expression in response to ethanol from published literature and we found that the expression of 52% of the genes with altered H3K4me3 binding and 40% of genes with H3K27me3 differences are altered by ethanol exposure. The chromatin changes associated with the 21-day post-exposure period suggest that this period is a unique state in the addiction cycle that differs from ethanol intoxication and acute withdrawal. These results provide insights into the enduring effects of ethanol on proteoglycan and calcium signaling genes in the brain.

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Ethanol-induced epigenetic regulations at the Bdnf gene in C57BL/6J mice

Cited by 53 publications

References 45 publications

Update of neurotrophic factors in neurobiology of addiction and future directions

Update of neurotrophic factors in neurobiology of addiction and future directions

Moderate-dose Regular Lifelong Alcohol Intake Changes the Intestinal Flora, Protects against Aging, and Keeps Spatial Memory in the Senescence-accelerated Mouse Prone 8 (SAMP8) Model

Stable Histone Methylation Changes at Proteoglycan Network Genes Following Ethanol Exposure

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