The impact of prenatal stress, fetal alcohol exposure, or both on development: perspectives from a primate model

Schneider, Mary L.; Moore, Colleen F.; Kraemer, Gary W.; Roberts, Andrew; DeJesus, Onofre T.

doi:10.1016/s0306-4530(01)00050-6

Cited by 183 publications

(146 citation statements)

References 58 publications

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“…However, caution should be taken in interpreting the increase of met-enkephalin levels in ET females since the increase was significantly different from IC females and not NTC females. The change may be due to a synergistic effect that can occur between early ethanol exposure and stress [33,41,44].…”

Section: Discussionmentioning

confidence: 99%

Perinatal ethanol exposure alters met-enkephalin levels of male and female rats

Lugo¹,

Wilson²,

Kelly³

2006

Neurotoxicology and Teratology

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This study used a rat model of Fetal Alcohol Syndrome to investigate whether combined prenatal and postnatal ethanol exposure affects met-enkephalin levels in the brains of male and female Long-Evans adult rats. Intragastric ethanol was administered to a group of rats (ET) from gestational day (GD) 1 through 22 and from postnatal day (PD) 2 through 10. The control groups consisted of a nontreated control group (NTC) and an intubated control group (IC) that received the intragastric intubation procedure but no exposure to ethanol. We measured met-enkephalin levels in the prefrontal cortex, nucleus accumbens, hypothalamus, central and basolateral nucleus of amygdala and ventral tegmental area. Met-enkephalin levels in the hypothalamus of male and female ET animals were significantly higher than those in either the NTC or IC animals. Metenkephalin levels in the central nucleus of the amygdala of male and female ET animals were significantly lower than the levels in the NTC animals. Met-enkephalin levels in the nucleus accumbens of ET females were significantly greater than those in the IC females. These results demonstrate that the combination of prenatal and postnatal ethanol exposure affects basal metenkephalin levels in specific regions in a sex-specific manner. These changes in met-enkephalin levels may explain how early ethanol exposure affects opioid-regulated behaviors such as social play, sexual behavior, and other social behaviors.

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Section: Discussionmentioning

confidence: 99%

Perinatal ethanol exposure alters met-enkephalin levels of male and female rats

Lugo¹,

Wilson²,

Kelly³

2006

Neurotoxicology and Teratology

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“…73). Interestingly, in rhesus monkeys, stress during pregnancy also programs increased HPA activity in the offspring (74). After the World Trade Center attacks of September 11, 2001, mothers who developed posttraumatic stress disorder showed lower cortisol levels, and most interestingly, so did their babies, with the effects mostly confined to those exposed in later pregnancy (29).…”

Section: Figurementioning

confidence: 99%

Prenatal dexamethasone exposure induces changes in nonhuman primate offspring cardiometabolic and hypothalamic-pituitary-adrenal axis function

Holmes²,

et al. 2007

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Prenatal stress or glucocorticoid administration has persisting "programming" effects on offspring in rodents and other model species. Multiple doses of glucocorticoids are in widespread use in obstetric practice. To examine the clinical relevance of glucocorticoid programming, we gave 50, 120, or 200 μg/kg/d of dexamethasone (dex50, dex120, or dex200) orally from mid-term to a singleton-bearing nonhuman primate, Chlorocebus aethiops (African vervet). Dexamethasone dose-dependently reduced maternal cortisol levels without effecting maternal blood pressure, glucose, electrolytes, or weight gain. Birth weight was unaffected by any dexamethasone dose, although postnatal growth was attenuated after dex120 and dex200. At 8 months of age, dex120 and dex200 offspring showed impaired glucose tolerance and hyperinsulinemia, with reduced (approximately 25%) pancreatic β cell number at 12 months. Dex120 and dex200 offspring had increased systolic and diastolic blood pressures at 12 months. Mild stress produced an exaggerated cortisol response in dex200 offspring, implying hypothalamic-pituitary-adrenal axis programming. The data are compatible with the extrapolation of the glucocorticoid programming hypothesis to primates and indicate that repeated glucocorticoid therapy and perhaps chronic stress in humans may have long-term effects.

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“…These effects are not limited to physical characteristics, but extend to a variety of behavioral traits. Thus, as described in several papers in this special issue and elsewhere, physical and emotional stressors experienced by pregnant rodent, monkey, and human females are associated with behavioral problems in offspring throughout life [1][2][3]. The physical and behavioral effects of prenatal stress appear to be mediated by hormoneinduced changes to the developing hypothalamic-pituitaryadrenal axis [3,4].…”

mentioning

confidence: 90%

Prenatal sex hormone effects on child and adult sex-typed behavior: methods and findings

Cohen-Bendahan

Beek

Berenbaum

2005

Neuroscience & Biobehavioral Reviews

485

400

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There is now good evidence that human sex-typed behavior is influenced by sex hormones that are present during prenatal development, confirming studies in other mammalian species. Most of the evidence comes from clinical populations, in which prenatal hormone exposure is atypical for a person's sex, but there is increasing evidence from the normal population for the importance of prenatal hormones. In this paper, we briefly review the evidence, focusing attention on the methods used to study behavioral effects of prenatal hormones. We discuss the promises and pitfalls of various types of studies, including those using clinical populations (concentrating on those most commonly studied, congenital adrenal hyperplasia, androgen insensitivity syndrome, ablatio penis, and cloacal exstrophy), direct measures of hormones in the general population (assayed through umbilical cord blood, amniotic fluid, and maternal serum during pregnancy), and indirect measures of hormones in the general population (inferred from intrauterine position and biomarkers such as otoacoustic emissions, finger length ratios, and dermatoglyphic asymmetries). We conclude with suggestions for interpreting and conducting studies of the behavioral effects of prenatal hormones. q

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The impact of prenatal stress, fetal alcohol exposure, or both on development: perspectives from a primate model

Cited by 183 publications

References 58 publications

Perinatal ethanol exposure alters met-enkephalin levels of male and female rats

Perinatal ethanol exposure alters met-enkephalin levels of male and female rats

Prenatal dexamethasone exposure induces changes in nonhuman primate offspring cardiometabolic and hypothalamic-pituitary-adrenal axis function

Prenatal sex hormone effects on child and adult sex-typed behavior: methods and findings

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