Maternal Alcohol Consumption and Stress Responsiveness in Offspring

Taylor, Anna N.; Branch, Berrilyn J.; Zuylen, J. E.; Redei, Eva E.

doi:10.1007/978-1-4899-2064-5_25

Cited by 51 publications

(36 citation statements)

References 16 publications

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“…In contrast, in the current study, suppressed HPT function was found only in the pair-fed and FAE females in response to prenatal T 4 treatment. This female specific vulnerability has been found previously for HPA function of offspring exposed prenatally to alcohol (56,60) or to stress (30,55).…”

Section: Discussionmentioning

confidence: 71%

Prenatal programming of adult thyroid function by alcohol and thyroid hormones

Wilcoxon

Redei

2004

American Journal of Physiology-Endocrinology and Metabolism

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Increasing evidence associates environmental challenges early in life with permanent alterations of physiological functions in adulthood. These changes in fetal environment can trigger physiological adaptations by the fetus, called fetal programming, which may be beneficial before birth but permanently influence the physiology of the organism. In this study, we investigated the potential connection between alcohol-induced decreased maternal thyroid function and the hypothalamic-pituitary-thyroid (HPT) function of adult rat offspring. Plasma 3,5,3'-triiodothyronine (T(3)), thyroxine (T(4)), and thyroid-stimulating hormone (TSH) levels were decreased in alcohol-consuming (E) dams on gestational day 21 compared with ad libitum- (C) and pair-fed (PF) controls. No significant differences were found in HPT function in young offspring (3 wk of age) between diet groups. However, adult fetal alcohol-exposed (FAE) offspring had significantly decreased levels of T(3) along with elevated TSH compared with control offspring. T(4) administration to the mother did not normalize the hypothyroid state of the adult FAE offspring. Interestingly, administration of T(4) to control pregnant dams decreased plasma T(3) of the adult female offspring only, whereas T(4) together with maternal alcohol consumption or pair-feeding led to decreased TSH and T(4) in the adult female offspring. Our results suggest that ethanol consumption and T(4) administration alter maternal HPT function, leading to prenatally programmed permanent alterations in the thyroid function of the adult offspring.

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Section: Discussionmentioning

confidence: 71%

Prenatal programming of adult thyroid function by alcohol and thyroid hormones

Wilcoxon

Redei

2004

American Journal of Physiology-Endocrinology and Metabolism

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“…31 This amount of ethanol-diet consumption is not different from the alcohol intake of dams of the same strain and age, which produced blood ethanol levels of 80 mg/100 ml at 0900 h and 127 mg/100 ml at 2000 h, as reported previously. 41 The body weight of alcohol-consuming dams was significantly lower than both of those on PF or control diets as described previously. 31 There was also a significant difference between the body weight of PF and control dams.…”

Section: Methodsmentioning

confidence: 77%

Behavioral deficits associated with fetal alcohol exposure are reversed by prenatal thyroid hormone treatment: a role for maternal thyroid hormone deficiency in FAE

et al. 2005

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Children prenatally exposed to alcohol typically exhibit behavioral abnormalities, including hyperactivity, learning deficits, and an increased prevalence of depression. Similar impairments are found in children of hypothyroid mothers, and we have shown that alcohol-consuming rat dams have suppressed hypothalamic-pituitary-thyroid (HPT) function. Therefore, we hypothesized that suppressed maternal thyroid hormonal milieu may contribute to the deleterious consequences of prenatal alcohol exposure. We aimed first to confirm and then to reverse the behavioral deficits in the fetal alcohol exposed (FAE) rat offspring by administration of thyroxine (T4) to the alcohol-consuming dams. Adult offspring prenatally exposed to ethanol (FAE; 35% ethanol-derived calories), pair-fed (PF) or control (C) diets were tested in the Morris water maze (MWM), the forced swim test (FST), and the open field test (OFT) to assess spatial learning, depressive behavior, and exploratory behavior/anxiety, respectively. Adult FAE offspring took longer to locate a hidden platform in the MWM and showed increased depressive behavior in the FST both of which were reversed by administration of T4 to the alcohol-consuming mother. We found sex and brain regionspecific alterations in expression of genes involved in these behaviors in FAE adult offspring. Specifically, decreased hippocampal GAP-43 mRNA levels in adult FAE females and decreased glucocorticoid receptor (GR) expression in the amygdala of male and female FAE offspring were observed. The decreased mRNA levels of GAP-43 and GR were normalized by T4 treatment to the alcohol-consuming mother. Our results suggest that the suppressed HPT function of the alcohol-consuming mother contributes to the behavioral and cognitive dysfunctions observed in the offspring. Prenatal alcohol exposure has long-term developmental consequences, 1-3 and in humans alcohol is recognized as a teratogen leading to long-lasting CNS dysfunctions. 4 Specifically, patients with fetal alcohol exposure (FAE) have marked cognitive deficits, including difficulty focusing and sustaining attention, 5 and place learning deficits in a virtual Morris water task. 6 Attention deficit hyperactivity disorder (ADHD) is frequently diagnosed in FAE children. These neurocognitive and behavioral characteristics differ between FAE children and those with a primary diagnosis of ADHD, as FAE children have difficulties primarily in the encoding and retrieval of information. 7 A significantly increased prevalence of depression is also found in children 8 and adults 9 prenatally exposed to alcohol. It is important to note that, in contrast to the higher female prevalence of depressive disorders in the general population, the rate of depression found in adults with prenatal alcohol exposure was nearly equal among men and women. 9 Fetal alcohol effects qualitatively similar to those described in children with a history of gestational alcohol exposure have been detected with animal models. 10 Cognitive deficits have been found in FAE animal models...

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“…This relationship seems to be mediated by different hormonal and neurochemical systems, such as the HPA axis and the pituitary Beta-endorphin system. Prenatal ethanol exposure alters levels of adrenocorticotropin hormone (ACTH) and corticosterone (Taylor et al, 1981;Taylor et al, 1988;Weinberg, 1989;Weinberg et al, 1996) as well as Beta-endorphins (Angelogianni and Gianoulakis, 1989) in response to different stressors. As mentioned earlier, in one study higher ethanol consumption was observed in rats prenatally exposed to the drug, but only after chronic stress (Nelson et al, 1983).…”

Section: Alterations In the Stress Responsementioning

confidence: 99%