Reduced expression of brain cannabinoid receptor 1 (Cnr1) is coupled with an increased complementary micro-RNA (miR-26b) in a mouse model of fetal alcohol spectrum disorders

Clinical Epigenetics

Shiva M Singh¹  Morgan L Kleiber¹  Benjamin I Laufer¹  Randa L Stringer¹ 

[1] Department of Biology, Molecular Genetics Unit, Western University, London, ON N6A 5B7, Canada

关键词: Prenatal alcohol exposure;    Neurodevelopment;    Mouse;    microRNA;    Gene regulation;    Epigenetics;    Cannabinoid receptor 1;   

Others  :  790913
DOI  :  10.1186/1868-7083-5-14

 received in 2013-05-07, accepted in 2013-06-28,  发布年份 2013

【 摘 要 】

Background

Prenatal alcohol exposure is known to result in fetal alcohol spectrum disorders, a continuum of physiological, behavioural, and cognitive phenotypes that include increased risk for anxiety and learning-associated disorders. Prenatal alcohol exposure results in life-long disorders that may manifest in part through the induction of long-term gene expression changes, potentially maintained through epigenetic mechanisms.

Findings

Here we report a decrease in the expression of Canabinoid receptor 1 (Cnr1) and an increase in the expression of the regulatory microRNA miR-26b in the brains of adult mice exposed to ethanol during neurodevelopment. Furthermore, we show that miR-26b has significant complementarity to the 3’-UTR of the Cnr1 transcript, giving it the potential to bind and reduce the level of Cnr1 expression.

Conclusions

These findings elucidate a mechanism through which some genes show long-term altered expression following prenatal alcohol exposure, leading to persistent alterations to cognitive function and behavioural phenotypes observed in fetal alcohol spectrum disorders.

【 授权许可】

   
2013 Stringer et al.; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

Figure 2.

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