In utero alcohol heightens juvenile reactivity

Anandam, Nirmala; Felegi, William; Stern, Judith M.

doi:10.1016/0091-3057(80)90276-2

Cited by 39 publications

(17 citation statements)

References 33 publications

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“…This sensitization to dopaminergic agonists and ethanol contrast with the tolerance reported when other indexes are measured. For example, greater tolerance has been observed to the hypothermic effects of ethanol (Abel et al, 1981;Anandam et al, 1980;Lancaster and Spiegel, 1989;Molina et al, 1987), with this index being related to the aversive effects of the drug (Cunningham et al, 1988;Hunt et al, 1991). Even though in these studies prenatal ethanol treatment does not alter the pharmacokinetics of the drug (Becker et al, 1993;Lancaster and Spiegel, 1989;Molina et al, 1987), an attenuated response to the aversive toxic properties of ethanol has been observed, along with a greater sensitivity to the stimulant reinforcing effects of the drug.…”

Section: Neurochemical Changesmentioning

confidence: 90%

Increased ethanol intake after prenatal ethanol exposure: Studies with animals

Chotro

Arias

Laviola

2007

Neuroscience & Biobehavioral Reviews

108

102

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Section: Neurochemical Changesmentioning

confidence: 90%

Increased ethanol intake after prenatal ethanol exposure: Studies with animals

Chotro

Arias

Laviola

2007

Neuroscience & Biobehavioral Reviews

108

102

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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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“…Studies using animal models to investigate the consequences of alcohol consumption during pregnancy on maternal care have reported inconsistent results. Some studies showed that alcohol during pregnancy did not alter maternal behavior (Anandam et al, 1980; Ewart and Cutler, 1979), others showed that pup retrieval was delayed or reduced (Abel, 1978; Ness and Franchina, 1990), and one on the combined exposure to alcohol and nicotine found increased time away from pups (McMurray et al, 2008). …”

Section: Introductionmentioning

confidence: 99%

Alcohol and pregnancy: Effects on maternal care, HPA axis function, and hippocampal neurogenesis in adult females

Workman

Raineki

Weinberg

et al. 2015

Psychoneuroendocrinology

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Chronic alcohol consumption negatively affects health, and has additional consequences if consumption occurs during pregnancy as prenatal alcohol exposure adversely affects offspring development. While much is known on the effects of prenatal alcohol exposure in offspring less is known about effects of alcohol in dams. Here, we examine whether chronic alcohol consumption during gestation alters maternal behavior, hippocampal neurogenesis and HPA axis activity in late postpartum female rats compared with nulliparous females. Rats were assigned to alcohol, pair-fed or ad libitum control treatment groups for 21 days (for pregnant rats, this occurred gestation days 1 – 21). Maternal behavior was assessed throughout the postpartum period. Twenty-one days after alcohol exposure, we assessed doublecortin (DCX) (an endogenous protein expressed in immature neurons) expression in the dorsal and ventral hippocampus and HPA axis activity. Alcohol consumption during pregnancy reduced nursing and increased self-directed and negative behaviors, but spared licking and grooming behavior. Alcohol consumption increased corticosterone and adrenal mass only in nulliparous females. Surprisingly, alcohol consumption did not alter DCX-expressing cell density. However, postpartum females had fewer DCX-expressing cells (and of these cells more immature proliferating cells but fewer postmitotic cells) than nulliparous females. Collectively, these data suggest that alcohol consumption during pregnancy disrupts maternal care without affecting HPA function or neurogenesis in dams. Conversely, alcohol altered HPA function in nulliparous females only, suggesting that reproductive experience buffers the long-term effects of alcohol on the HPA axis.

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In utero alcohol heightens juvenile reactivity

Cited by 39 publications

References 33 publications

Increased ethanol intake after prenatal ethanol exposure: Studies with animals

Increased ethanol intake after prenatal ethanol exposure: Studies with animals

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

Alcohol and pregnancy: Effects on maternal care, HPA axis function, and hippocampal neurogenesis in adult females

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