Early gestational exposure to moderate concentrations of ethanol alters adult behaviour in C57BL/6J mice

Vega, M.C.; Chong, Suyinn; Burne, Thomas H. J.

doi:10.1016/j.bbr.2013.06.003

Cited by 40 publications

(42 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The exposure window utilised in this model is developmentally equivalent to the first 3 -4 weeks of a human pregnancy (Otis and Brent, 1954) -well before most Australian women will confirm their pregnancies (Callinan and Room, 2012). It has previously been identified using this model, that ethanol exposure even when restricted to this very early time in pregnancy was sufficient to result in changes to behaviour (Sanchez Vega et al, 2013), brain structure (Marjonen et al, 2015), craniofacial morphology (Kaminen-Ahola et al, 2010b), and postnatal growth (Kaminen-Ahola et al, 2010a).…”

Section: Consequences Of Early Gestational Exposure To Ethanol And/ormentioning

confidence: 99%

“…In addition to these, the usage of animal models has allowed for the investigation of a wide range of other phenotypes resultant of prenatal ethanol exposure: impairments to behaviour (Sanchez Vega et al, 2013), glucose metabolism (Harper et al, 2014), adiposity (Dobson et al, 2012), renal (Gray et al, 2010) and cardiovascular (Ren et al, 2002) function, lung development (Probyn et al, 2013), hypothalamic-pituitary-adrenal function (Lan et al, 2009), and even osteoarthritis risk (Ni et al, 2015).…”

Section: Evidence In Animal Modelsmentioning

confidence: 99%

“…The prenatal ethanol exposure model used in this project is as previously described (Kaminen-Ahola et al, 2010a,b;Sanchez Vega et al, 2013). During the exposure period from 0.5 to 8.5 dpc, ethanoltreated dams were provided with ad libitum access to 10% (v/v) non-denatured ethanol.…”

Section: Prenatal Exposure To Ethanol And/or Nicotinementioning

confidence: 99%

“…These phenotypes include abnormal neural development and behaviour (Sanchez Vega et al, 2013;Zhang et al, 2015), growth retardation (Kaminen-Ahola et al, 2010b;Probyn et al, 2012;Gardebjer et al, 2014) and craniofacial abnormalities (Sulik et al, 1981;Anthony et al, 2010;Kaminen-Ahola et al, 2010b), metabolic perturbations (Dobson et al, 2012;Harper et al, 2014), as well as the abnormal development and function of the renal, cardiovascular and pulmonary systems (Ren et al, 2002;Gray et al, 2010;Probyn et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

“…The ethanol-only model used in this thesis was previously established by our laboratory (KaminenAhola et al, 2010b,a;Sanchez Vega et al, 2013;Zhang et al, 2015). One of the mechanisms by which gestational environment is hypothesised to program subsequent health is by the impairment of organogenesis, leading to impaired organ function and thus disease later in life (Desai and Hales, 1997;Ingelfinger and Woods, 2002;Hyatt et al, 2008).…”

mentioning

confidence: 99%

See 4 more Smart Citations

A study of the consequences of early gestational ethanol and/or nicotine exposure in the mouse

Yamada¹

View full text Add to dashboard Cite

The in utero environment is a critical determinant of the immediate and future health of the developing fetus. In Australia, two of the most commonly used drugs during pregnancy are alcohol and nicotine. Prolonged periods of gestational exposure to alcohol and nicotine, separately, have been associated with a range of adverse outcomes in the offspring, in both humans and experimental animal models. The consequences of ethanol and nicotine exposure restricted to early gestation on resultant offspring are poorly characterised, and few animal models exist to build greater understanding. Moreover, the immediate molecular changes associated with exposures to ethanol and/or nicotine restricted to early gestation has yet to be described.This thesis utilised mouse models of early gestational ethanol and/or nicotine exposure to explore the impact of each of these exposures on offspring growth, as well as their associated transcriptional and epigenetic changes. In each model, pregnant C57BL/6 dams were provided with ad libitum access to solutions of 10% ethanol and/or 100 µg/ml nicotine from fertilisation (0.5 dpc) to midgestation (8.5 dpc). The exposure window utilised in each of the models is developmentally equivalent to the first three to four weeks of a human pregnancy.Previously, our laboratory identified reduced growth, microcephaly, and gene expression changes in the liver and hippocampus of the postnatal offspring of the model of prenatal ethanol exposure utilised in this thesis. In contrast, at mid-gestation (9.5 dpc), there was no evidence of developmental delay (somite number), reduced growth (crown-rump length), or microcephaly.Further, a genome-wide gene expression microarray (targeting 30 855 genes) and a screen of the expression of 641 microRNAs, identified only one gene (Bcl11b) as differentially expressed in male 9.5 dpc whole embryos following the ethanol exposure. These data suggest that there is a delay between the ethanol exposure and the onset of adverse phenotypes -arguing that the embryo is somehow able to form a memory of the ethanol exposure. The absence of widespread transcriptional changes suggests that changes in embryonic mRNA and microRNA expression are unlikely to be major contributors to the memory of the exposure.A early gestational model of nicotine exposure was newly established in this thesis. This nicotine exposure resulted in an average serum cotinine (metabolite of nicotine) concentration similar to that reported in humans who smoke 10 to 15 cigarettes per day. This exposure was sufficient to induce a reduction in body size both at mid-gestation and postnatally, but not at late gestation. Furthermore, the increased expression of Zscan10 in the whole male 9.5 dpc embryo was identified and validated across multiple cohorts. Zscan10 encodes for a transcription factor expressed throughout development, with a proposed role in the regulation of progenitor cells. The increased expression of Zscan10 in the nicotine-exposed embryos was associated with a reduction in DNA methylation ...

show abstract

Section: Consequences Of Early Gestational Exposure To Ethanol And/ormentioning

confidence: 99%

Section: Evidence In Animal Modelsmentioning

confidence: 99%

Section: Prenatal Exposure To Ethanol And/or Nicotinementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

A study of the consequences of early gestational ethanol and/or nicotine exposure in the mouse

Yamada¹

View full text Add to dashboard Cite

show abstract

Exploring behavioral phenotypes in a mouse model of fetal alcohol spectrum disorders

Chaudoin

Bonasera

Dunaevsky

et al. 2023

Developmental Neurobiology

View full text Add to dashboard Cite

Fetal alcohol spectrum disorders are one of the leading causes of developmental abnormalities worldwide. Maternal consumption of alcohol during pregnancy leads to a diverse range of cognitive and neurobehavioral deficits. Although moderate‐to‐heavy levels of prenatal alcohol exposure (PAE) have been associated with adverse offspring outcomes, there is limited data on the consequences of chronic low‐level PAE. Here, we use a model of maternal voluntary alcohol consumption throughout gestation in a mouse model to investigate the effects of PAE on behavioral phenotypes during late adolescence and early adulthood in male and female offspring. Body composition was measured by dual‐energy X‐ray absorptiometry. Baseline behaviors, including feeding, drinking, and movement, were examined by performing home cage monitoring studies. The impact of PAE on motor function, motor skill learning, hyperactivity, acoustic reactivity, and sensorimotor gating was investigated by performing a battery of behavioral tests. PAE was found to be associated with altered body composition. No differences in overall movement, food, or water consumption were observed between control and PAE mice. Although PAE offspring of both sexes exhibited deficits in motor skill learning, no differences were observed in basic motor skills such as grip strength and motor coordination. PAE females exhibited a hyperactive phenotype in a novel environment. PAE mice exhibited increased reactivity to acoustic stimuli, and PAE females showed disrupted short‐term habituation. Sensorimotor gating was not altered in PAE mice. Collectively, our data show that chronic low‐level exposure to alcohol in utero results in behavioral impairments.

show abstract

Fetal alcohol spectrum disorders: Genetic and epigenetic mechanisms

Kaminen‐Ahola

2020

Prenatal Diagnosis

View full text Add to dashboard Cite

Fetal alcohol spectrum disorders (FASD) are a consequence of prenatal alcohol exposure (PAE). The etiology of the complex FASD phenotype with growth deficit, birth defects, and neurodevelopmental impairments is under extensive research. Both genetic and environmental factors contribute to the wide phenotype: chromosomal rearrangements, risk and protective alleles, environmental‐induced epigenetic alterations as well as gene‐environment interactions are all involved. Understanding the molecular mechanisms of PAE can provide tools for prevention or intervention of the alcohol‐induced developmental disorders in the future. By revealing the alcohol‐induced genetic and epigenetic alterations which associate with the variable FASD phenotypes, it is possible to identify biomarkers for the disorder. This would enable early diagnoses and personalized support for development of the affected child.

show abstract

Early gestational exposure to moderate concentrations of ethanol alters adult behaviour in C57BL/6J mice

Cited by 40 publications

References 63 publications

A study of the consequences of early gestational ethanol and/or nicotine exposure in the mouse

A study of the consequences of early gestational ethanol and/or nicotine exposure in the mouse

Exploring behavioral phenotypes in a mouse model of fetal alcohol spectrum disorders

Fetal alcohol spectrum disorders: Genetic and epigenetic mechanisms

Contact Info

Product

Resources

About