Maternal ethanol consumption and hyperactivity in cross-fostered offspring

Martin, Joan C.; Martin, Donald C.; Sigman, Gary; Radow, Barbara

doi:10.3758/bf03326739

Cited by 47 publications

(10 citation statements)

References 17 publications

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“…These include retarded pre- and post-natal growth and development, physical malformations, CNS abnormalities (Abel and Dintcheff, 1978; Chernoff, 1977; Druse, 1996; Leichter and Lee, 1979; Randall, Taylor, and Walker, 1977; Weinberg, 1993; Weinberg and Gallo, 1982), and a wide range of behavioral and cognitive deficits, including deficits in learning and memory, hyperactivity, hyper-responsivity to stressors, and deficits in both response inhibition and appropriate use of environmental cues (Abel, 1979; Anandam, Felegi, and Stern, 1980; Bond and Di Giusto, 1976; Bond and Digiusto, 1977; Gallo and Weinberg, 1982; Kim et al, 1997; Lochry and Riley, 1980; Martin, Martin, Sigman, and Radow, 1978; Riley, Baron, and Hannigan, 1986; Riley, Lochry, and Shapiro, 1979; Weinberg, 1992b). …”

Section: Fetal Alcohol Spectrum Disorder (Fasd)mentioning

confidence: 99%

Prenatal alcohol exposure: Fetal programming and later life vulnerability to stress, depression and anxiety disorders

Hellemans

Śliwowska

Verma

et al. 2010

Neuroscience & Biobehavioral Reviews

295

232

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Children with Fetal Alcohol Spectrum Disorder (FASD) exhibit cognitive, neuropsychological and behavioral problems, and numerous secondary disabilities including depression and anxiety disorders. Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis is common in depression/anxiety, reflected primarily in increased HPA tone or activity. Prenatal alcohol exposure (PAE) increases HPA tone and results in HPA dysregulation throughout life, paralleling many of the HPA changes in depression/anxiety. We review data demonstrating altered HPA function and increased depression/anxiety in FASD. In the context of the stress-diathesis model, we discuss the hypothesis that fetal programming of the HPA axis by PAE alters neuroadaptive mechanisms that mediate the stress response, thus sensitizing the organism to stressors encountered later in life, and mediating, at least partly, the increased vulnerability to depression/anxiety disorders. Furthermore, we present evidence demonstrating sex-specific alterations in both hormonal and behavioral responsiveness to tasks measuring depressive- and anxiety-like behaviors in PAE offspring. Overall, the research suggests that the stress-diathesis model provides a powerful approach for elucidating mechanisms underlying the increased vulnerability to mental illness among individuals with FASD, and developing appropriate treatments for these individuals. Dr. Seymour Levine’s seminal work on the long-term consequences of early life experiences formed a framework for the development of the research described in this review.

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Section: Fetal Alcohol Spectrum Disorder (Fasd)mentioning

confidence: 99%

Prenatal alcohol exposure: Fetal programming and later life vulnerability to stress, depression and anxiety disorders

Hellemans

Śliwowska

Verma

et al. 2010

Neuroscience & Biobehavioral Reviews

295

232

View full text Add to dashboard Cite

show abstract

“…retarded pre and postnatal growth and development, physical malformations, and CNS abnormalities) (7, 31–36). Studies have also reported physiological abnormalities such as altered hormonal and immune function (8, 14, 15), as well as a wide range of cognitive and behavioural changes, including hyperactivity, hyper‐responsivity to stressors, deficits in response inhibition, and deficits in appropriate use of environmental cues (37–47). These findings are a correlate of the cognitive and behavioural abnormalities observed in alcohol‐exposed children.…”

Section: Foetal Alcohol Spectrum Disorder: Description In Human and Amentioning

confidence: 99%

Prenatal Alcohol Exposure: Foetal Programming, the Hypothalamic‐Pituitary‐Adrenal Axis and Sex Differences in Outcome

Weinberg

Śliwowska

et al. 2008

J Neuroendocrinology

287

263

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Prenatal exposure to alcohol has adverse effects on offspring neuroendocrine and behavioural functions. Alcohol readily crosses the placenta, thus directly affecting developing foetal endocrine organs. In addition, alcohol‐induced changes in maternal endocrine function can disrupt the normal hormonal interactions between the pregnant female and foetal systems, altering the normal hormone balance and, indirectly, affecting the development of foetal metabolic, physiological and endocrine functions. The present review focuses on the adverse effects of prenatal alcohol exposure on offspring neuroendocrine function, with particular emphasis on the hypothalamic‐pituitary‐adrenal (HPA) axis, a key player in the stress response. The HPA axis is highly susceptible to programming during foetal and neonatal development. Here, we review data demonstrating that alcohol exposure in utero programmes the foetal HPA axis such that HPA tone is increased throughout life. Importantly, we show that, although alterations in HPA responsiveness and regulation are robust phenomena, occurring in both male and female offspring, sexually dimorphic effects of alcohol are frequently observed. We present updated findings on possible mechanisms underlying differential effects of alcohol on male and female offspring, with special emphasis on effects at different levels of the HPA axis, and on modulatory influences of the hypothalamic–pituitary–gonadal hormones and serotonin. Finally, possible mechanisms underlying foetal programming of the HPA axis, and the long‐term implications of increased exposure to endogenous glucocorticoids for offspring vulnerability to illnesses or disorders later in life are discussed.

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“…For example, in rodents, alcohol exposure in utero results in retarded intrauterine and postnatal growth (Henderson & Schenker, 1977;Martin, Martin, Sigman, & Radow, 1977;Riley, Lochry, Shapiro, & Baldwin, 1979;Tze & Lee, 1975) as weII as delayed behavioral development (Demers & Kirouac, 1978;Shaywitz, Klopper, & Gordon, 1976). The most commonly reported behavioral consequence of prenatal alcohol exposure is hyperactivity as measured in an open field tBond & DiGiusto, 1976DiGiusto, , 1977Branchey & Friedhoff, 1976;Shaywitz et aI., 1976) and running wheel (Martin, Martin, Sigman, & Radow, 1978). However, hyperactive behavior is by no means the sole manifestation of prenatal alcohol exposure.…”

mentioning

confidence: 99%

Fixed-ratio performance and subsequent extinction in rats prenatally exposed to ethanol

et al. 1980

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Pregnant Long-Evan rats were fed isocaloric liquid diets containing 35%, 23%, 11 %, or 0% ethanol-derived calories (EDC) from Day 5 to Day 20 of gestation. Shortly after weaning, male offspring of these mothers were tested for the acquisition and extinction of a fixed-ratio (FR) barpress response. As the schedule requirement was progressively increased from FR 2 to FR 33, the 35% (EDC) offspring consistently had the lowest response rates, 23% and 11 % (EDC) offspring were intermediate, and the 0% (EDC) progeny had the highest response rates (p < .01), During extinction, this pattern was reversed; the number of responses increased as a function of prenatal alcohol exposure (p < .025).

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Maternal ethanol consumption and hyperactivity in cross-fostered offspring

Cited by 47 publications

References 17 publications

Prenatal alcohol exposure: Fetal programming and later life vulnerability to stress, depression and anxiety disorders

Prenatal alcohol exposure: Fetal programming and later life vulnerability to stress, depression and anxiety disorders

Prenatal Alcohol Exposure: Foetal Programming, the Hypothalamic‐Pituitary‐Adrenal Axis and Sex Differences in Outcome

Fixed-ratio performance and subsequent extinction in rats prenatally exposed to ethanol

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