Periconceptional maternal alcohol consumption leads to behavioural changes in adult and aged offspring and alters the expression of hippocampal genes associated with learning and memory and regulators of the epigenome

Lucia, D.; Burgess, D. J.; Cullen, Carlie L.; Dorey, Emily S.; Rawashdeh, Oliver

doi:10.1016/j.bbr.2019.01.009

Cited by 16 publications

(13 citation statements)

References 45 publications

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“…The experimental differences may account for the discrepancies in outcomes described in the literature. The gene expression changes following PAE and ELS accompany comprehensive demonstration that different regimes of PAE result in genome-wide changes in brain gene expression in rodents at different stages of neurodevelopment (Kleiber et al, 2012(Kleiber et al, , 2013Mantha et al, 2014;Gangisetty et al, 2015;Chastain et al, 2019;Lucia et al, 2019;Ieraci and Herrera, 2020;Shivakumar et al, 2020). As gene expression changes likely underlie changes in behavior, the focus becomes on mechanisms of gene expression regulation throughout neurodevelopment.…”

Section: Modeling Fasd Including Els In Rodentsmentioning

confidence: 99%

Epigenetic Impacts of Early Life Stress in Fetal Alcohol Spectrum Disorders Shape the Neurodevelopmental Continuum

Alberry

Laufer

Chater‐Diehl

et al. 2021

Front. Mol. Neurosci.

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Neurodevelopment in humans is a long, elaborate, and highly coordinated process involving three trimesters of prenatal development followed by decades of postnatal development and maturation. Throughout this period, the brain is highly sensitive and responsive to the external environment, which may provide a range of inputs leading to positive or negative outcomes. Fetal alcohol spectrum disorders (FASD) result from prenatal alcohol exposure (PAE). Although the molecular mechanisms of FASD are not fully characterized, they involve alterations to the regulation of gene expression via epigenetic marks. As in the prenatal stages, the postnatal period of neurodevelopment is also sensitive to environmental inputs. Often this sensitivity is reflected in children facing adverse conditions, such as maternal separation. This exposure to early life stress (ELS) is implicated in the manifestation of various behavioral abnormalities. Most FASD research has focused exclusively on the effect of prenatal ethanol exposure in isolation. Here, we review the research into the effect of prenatal ethanol exposure and ELS, with a focus on the continuum of epigenomic and transcriptomic alterations. Interestingly, a select few experiments have assessed the cumulative effect of prenatal alcohol and postnatal maternal separation stress. Regulatory regions of different sets of genes are affected by both treatments independently, and a unique set of genes are affected by the combination of treatments. Notably, epigenetic and gene expression changes converge at the clustered protocadherin locus and oxidative stress pathway. Functional studies using epigenetic editing may elucidate individual contributions of regulatory regions for hub genes and further profiling efforts may lead to the development of non-invasive methods to identify children at risk. Taken together, the results favor the potential to improve neurodevelopmental outcomes by epigenetic management of children born with FASD using favorable postnatal conditions with or without therapeutic interventions.

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Section: Modeling Fasd Including Els In Rodentsmentioning

confidence: 99%

Epigenetic Impacts of Early Life Stress in Fetal Alcohol Spectrum Disorders Shape the Neurodevelopmental Continuum

Alberry

Laufer

Chater‐Diehl

et al. 2021

Front. Mol. Neurosci.

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“…Specifically, in a study conducted by Burgess et al , female rat progeny exposed to periconceptional alcohol demonstrated significant decreases in basal corticosterone levels, as well as significant increases in levels of hippocampal GR gene expression . A separate study by Lucia et al investigating a similar paradigm found subtle increases in anxiety‐like behaviour and short‐term spatial memory impairment in female rat progeny exposed to periconceptional alcohol . These observations are of particular relevance given that a majority of women who drink alcohol during pregnancy stop once they are pregnant but still potentially expose the foetus to alcohol during a critical neurodevelopmental period and thus inadvertently increase susceptibility of offspring to aberrant HPA axis function and stress responses.…”

Section: Prenatal Exposure To Select Drugs Of Abuse Leads To Altered mentioning

confidence: 96%

Prenatal drug exposure and neurodevelopmental programming of glucocorticoid signalling

Franks

Berry

DeFranco

2019

J Neuroendocrinology

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Prenatal neurodevelopment is dependent on precise functioning of multiple signalling pathways in the brain, including those mobilised by glucocorticoids (GC) and endocannabinoids (eCBs). Prenatal exposure to drugs of abuse, including opioids, alcohol, cocaine and cannabis, has been shown to not only impact GC signalling, but also alter functioning of the hypothalamic‐pituitary‐adrenal (HPA) axis. Such exposures can have long‐lasting neurobehavioural consequences, including alterations in the stress response in the offspring. Furthermore, cannabis contains cannabinoids that signal via the eCB pathway, which is linked to some components of GC signalling in the adult brain. Given that GCs are frequently used in pregnancy to prevent complications of prematurity, and also that rates of cannabis use in pregnancy are increasing, the likelihood of foetal co‐exposure to these compounds is high and may have additional implications for long‐term neurodevelopment. Here, we present a discussion of GC signalling and the HPA axis, as well as the effects of prenatal drug exposure on these pathways and the stress response, and we explore the interactions between GC and EC signalling in the developing brain and potential for neurodevelopmental consequences.

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“…Mooney et al demonstrated that following an intravenous treatment with 20% v/v (a BAL of 233 ± 7.5 mg/dL) alcohol on E7 only, male Long-Evans rat offspring had greater social interaction than those not exposed to alcohol 124 , potentially indicating hyperactivity and/or altered awareness of social cues. Periconceptional ethanol exposure in a Sprague-Dawley rat model (12.5% ethanol, a BAL of 180 ± 40 mg/dL, liquid diet), highly relevant due to the high incidence of unplanned pregnancy, has also been shown to programme sex-specific spatial memory deficits and anxiety-like behaviours 125 .…”

Section: Animal Models Of Prenatal Alcohol Exposure and Mental Illnessmentioning

confidence: 99%

Prenatal alcohol exposure and developmental programming of mental illness

Burgess

2020

J Dev Orig Health Dis

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It is well established that high-dose alcohol consumption during pregnancy increases the risk for a plethora of adverse offspring outcomes. These include neurodevelopmental, cognitive and social deficits, as well as psychiatric illnesses, such as depression and anxiety. However, much less evidence is available on the effects of low- and early-dose alcohol exposure on mental health outcomes, regardless of the accumulating evidence that mental health outcomes should be considered in the context of the Developmental Origins of Health and Disease hypothesis. This review will discuss the evidence that indicates low-dose and early prenatal alcohol exposure can increase the risk of mental illness in offspring and discuss the mechanistic pathways that may be involved.

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Periconceptional maternal alcohol consumption leads to behavioural changes in adult and aged offspring and alters the expression of hippocampal genes associated with learning and memory and regulators of the epigenome

Cited by 16 publications

References 45 publications

Epigenetic Impacts of Early Life Stress in Fetal Alcohol Spectrum Disorders Shape the Neurodevelopmental Continuum

Epigenetic Impacts of Early Life Stress in Fetal Alcohol Spectrum Disorders Shape the Neurodevelopmental Continuum

Prenatal drug exposure and neurodevelopmental programming of glucocorticoid signalling

Prenatal alcohol exposure and developmental programming of mental illness

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