Effects of Prenatal Exposure to Alcohol on the Release of Adenocorticotropic Hormone, Corticosterone, and Proinflammatory Cytokines

Kim, C. Kwon; Turnbull, Andrew V.; Lee, Soon Y.; Rivier, Catherine

doi:10.1097/00000374-199901000-00008

Cited by 13 publications

(17 citation statements)

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“…In studies to date, including our own, HPA hormone levels have been measured primarily at the circadian trough, and typically without regard to estrous cycle stage (Kim et al, 1999; Lee and Rivier, 1996; Weinberg, 1988; 1992a). In the present report, by factoring in stage of estrous cycle, we unmasked differences in basal CORT among prenatal groups, and found that basal CORT levels varied as a function of prenatal treatment and estrous cycle stage.…”

Section: Discussionmentioning

confidence: 99%

Effects of prenatal ethanol exposure on regulation of basal hypothalamic–pituitary–adrenal activity and hippocampal 5-HT1A receptor mRNA levels in female rats across the estrous cycle

Śliwowska

Yamashita

et al. 2008

Psychoneuroendocrinology

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Summary Prenatal ethanol exposure, like other early adverse experiences, is known to alter hypothalamic-pituitary-adrenal (HPA) activity in adulthood. The present study examined the modulatory effects of the gonadal hormones on basal HPA regulation and serotonin type 1A receptor (5-HT1A) levels in adult female rats prenatally exposed to ethanol (E) compared to that in females from pair-fed (PF) and ad libitum-fed control (C) conditions. We demonstrate, for the first time, long-lasting consequences of prenatal ethanol exposure for basal corticosterone (CORT) regulation and basal levels of hippocampal mineralocorticoid (MR), glucocorticoid (GR) and serotonin type 1A (5-HT1A) receptor mRNA, as a function of estrous cycle stage: 1) basal CORT levels were higher in E compared to C females in proestrus but lower in E and PF compared to C females in estrus; 2) there were no differences among groups in basal levels of adrenocorticotropin (ACTH), estradiol or progesterone; 3) hippocampal MR mRNA levels were decreased in E compared to PF and C females across the estrus cycle, with the greatest effects in proestrus, whereas E (but not PF or C) females had higher hippocampal GR mRNA levels in proestrus than in estrous and diestrus; 4) 5-HT1A mRNA levels were increased in E compared to PF and C females in diestrus. That alterations were revealed as a function of estrous cycle stage suggests a role for the ovarian steroids in mediating the adverse effects of ethanol. Furthermore, it appears that ethanol-induced nutritional effects may play a role in mediating at least some of the effects observed. The resetting of HPA activity by early environmental events could be one mechanism linking early life experiences with long-term health consequences. Thus, changes in basal CORT levels, a shift in the MR/GR balance and alterations in 5-HT1A receptor mRNA could have important clinical implications for understanding the secondary disabilities, such as an increased incidence of depression, in children with FASD.

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Section: Discussionmentioning

confidence: 99%

Effects of prenatal ethanol exposure on regulation of basal hypothalamic–pituitary–adrenal activity and hippocampal 5-HT1A receptor mRNA levels in female rats across the estrous cycle

Śliwowska

Yamashita

et al. 2008

Psychoneuroendocrinology

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“…Interestingly, while HPA hyperresponsiveness is a robust phenomenon, sex differences in response are often observed depending on the nature and intensity of the stressor, time course of testing, and hormonal endpoint measured (Weinberg, 1985; Weinberg, 1992a; Weinberg, Taylor, and Gianoulakis, 1996; Weinberg et al, 2008). For example, both PAE males and females exhibit increased CORT, ACTH and/or β-EP (Weinberg, 1988; Weinberg, 1992a; Weinberg et al, 1996), as well as increased immediate early gene and CRH mRNA levels (Kim, Turnbull, Lee, and Rivier, 1999; Lee, Imaki, Vale, and Rivier, 1990; Lee, Schmidt, Tilders, and Rivier, 2000; Gabriel, Glavas, Ellis, and Weinberg 2005), in response to stressors such as repeated restraint, footshock, and immune challenges. PAE males and females also both show deficits in habituation to repeated restraint, although patterns of response may differ for the different HPA hormones measured (Weinberg et al, 1996).…”

Section: Prenatal Alcohol Exposure and Hpa Dysregulationmentioning

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

291

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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“…Animal models of prenatal alcohol exposure (PAE) support and extend the clinical findings. Increased susceptibility to infections (Grossmann et al, 1993; McGill et al, 2009) and malignancies (Gottesfeld and Abel, 1991), deficits in immune organ development (Bray et al, 1993; Ewald and Frost, 1987; Ewald and Walden, 1988; Redei et al, 1989), decreased splenic lymphocyte, T lymphoblast, and B cell proliferative responses to stimulation (Gottesfeld et al, 1990; Jerrells and Weinberg, 1998; Weinberg and Jerrells, 1991; Wolcott et al, 1995), blunted LPS-induced febrile responses (Taylor et al, 1999), dampened cytokine responses to immune challenge (Chiappelli et al, 1997; Kim et al, 1999; Lee and Rivier, 1993), and a more severe and prolonged course of inflammation in an adjuvant-induced arthritis model (Zhang et al, 2012) have been reported in models of in utero alcohol exposure [reviewed in Bodnar and Weinberg 2013].…”

Section: Introductionmentioning

confidence: 99%

Evidence for an immune signature of prenatal alcohol exposure in female rats

Bodnar

Hill

Weinberg

2016

Brain, Behavior, and Immunity

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Evidence for immune/neuroimmune disturbances as a possible root cause of a range of disorders, including neurodevelopmental disorders, is growing. Although prenatal alcohol exposure (PAE) impacts immune function, few studies to date have examined immune function in relation to long-term negative health outcomes following PAE, and most have focused on males. To fill this gap, we utilized a rat model to examine the effects of PAE on immune/neuroimmune function during early-life [birth (postnatal day 1; P1), P8, and weaning (P22)] in PAE and control females. Due to the extensive interplay between the immune and endocrine systems, we also measured levels of corticosterone and corticosterone binding globulin (CBG). While corticosterone levels were not different among groups, CBG levels were lower in PAE offspring from P1–P8, suggesting a lower corticosterone reservoir that may underlie susceptibility to inflammation. Spleen weights were increased in PAE rats on P22, a marker of altered immune function. Moreover, we detected a unique cytokine profile in PAE compared to control offspring on P8 – higher levels in the PFC and hippocampus, and lower levels in the hypothalamus and spleen. The finding of a specific immune signature in PAE offspring during a sensitive developmental period has important implications for understanding the basis of long-term immune alterations and health outcomes in children with Fetal Alcohol Spectrum Disorder (FASD). Our findings also highlight the future possibility that immune-based intervention strategies could be considered as an adjunctive novel therapeutic approach for individuals with FASD.

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Effects of Prenatal Exposure to Alcohol on the Release of Adenocorticotropic Hormone, Corticosterone, and Proinflammatory Cytokines

Cited by 13 publications

References 0 publications

Effects of prenatal ethanol exposure on regulation of basal hypothalamic–pituitary–adrenal activity and hippocampal 5-HT1A receptor mRNA levels in female rats across the estrous cycle

Effects of prenatal ethanol exposure on regulation of basal hypothalamic–pituitary–adrenal activity and hippocampal 5-HT1A receptor mRNA levels in female rats across the estrous cycle

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

Evidence for an immune signature of prenatal alcohol exposure in female rats

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