title: 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.
abstract: 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.
  
  
  RESULTS
  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.
authors.affiliation: Department of Biology, Molecular Genetics Unit, Western University, London, ON N6A 5B7, Canada. ssingh@uwo.ca.
authors.forename: Randa L
authors.initials: RL
authors.lastname: Stringer
authors.forename: Benjamin I
authors.initials: BI
authors.lastname: Laufer
authors.forename: Morgan L
authors.initials: ML
authors.lastname: Kleiber
authors.forename: Shiva M
authors.initials: SM
authors.lastname: Singh
references.citation: Toxicol Sci. 2012 May;127(1):18-28
references.pmid: 22298809
references.citation: Nat Genet. 2011 Aug 21;43(9):854-9
references.pmid: 21857679
references.citation: Neuropharmacology. 2011 Dec;61(7):1160-5
references.pmid: 21251919
references.citation: J Cell Biochem. 2012 Nov;113(11):3455-65
references.pmid: 22678827
references.citation: Acta Psychiatr Scand. 2011 Oct;124(4):250-61
references.pmid: 21916860
references.citation: J Neurodev Disord. 2013 Mar 13;5(1):6
references.pmid: 23497526
references.citation: Int J Obes (Lond). 2006 Apr;30 Suppl 1:S13-8
references.pmid: 16570099
references.citation: Science. 2000 Feb 11;287(5455):1056-60
references.pmid: 10669420
references.citation: Neurobiol Dis. 2004 Dec;17(3):403-14
references.pmid: 15571976
references.citation: Genome Res. 2009 Jan;19(1):92-105
references.pmid: 18955434
references.citation: Dev Disabil Res Rev. 2009;15(3):176-92
references.pmid: 19731384
references.citation: CMAJ. 2005 Mar 1;172(5 Suppl):S1-S21
references.pmid: 15738468
references.citation: PLoS One. 2011;6(12):e28656
references.pmid: 22194877
references.citation: Dis Model Mech. 2013 Jul;6(4):977-92
references.pmid: 23580197
references.citation: Neuroscience. 2012 Mar 1;204:230-44
references.pmid: 21920410
references.citation: Hum Reprod. 2009 Mar;24(3):562-79
references.pmid: 19091803
references.citation: Philos Trans R Soc Lond B Biol Sci. 2001 Mar 29;356(1407):381-408
references.pmid: 11316486
references.citation: Genes Dev. 2012 Jan 1;26(1):25-30
references.pmid: 22215807
references.citation: Ann N Y Acad Sci. 2008 Nov;1144:154-75
references.pmid: 19076375
references.citation: J Atten Disord. 2006 Feb;9(3):515-22
references.pmid: 16481668