Effect of prenatal exposure to ethanol on the activity of the hypothalamic-pituitary-adrenal axis of the offspring: Importance of the time of exposure to ethanol and possible modulating mechanisms☆
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Role of corticosterone in anxiety- and depressive-like behavior and HPA regulation following prenatal alcohol exposure
2019, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :PAE rats older than 3–5 days of age, however, typically show basal CORT levels comparable to those in control rats (Glavas et al., 2007; Kim et al., 1999b; Lam et al., 2018a; Nelson et al., 1986; Uban et al., 2013; Weinberg et al., 1996). In response to a wide range of stressors, PAE typically (with the exception of the stress hyporesponsive period) increases HPA activation and/or delayed return to basal CORT levels compared to control animals, and effects are often sex- and stressor-dependent (Angelogianni and Gianoulakis, 1989; Giberson et al., 1997; Kim et al., 1999a; Lee et al., 1990, 2000; Lee and Rivier, 1996; Nelson et al., 1986; Redei et al., 1993; Taylor et al., 1981, 1982; Weinberg, 1988, 1992a, 1992b; Weinberg et al., 1996, 2008). Studies in humans have also reported that PAE increases both basal (Jacobson et al., 1999; Ramsay et al., 1996) and stress (Haley et al., 2006; Jacobson et al., 1999; Ouellet-Morin et al., 2011) levels of cortisol.
The Corticotropin Releasing Factor System and Alcohol Consumption
2016, Molecular Aspects of Alcohol and Nutrition: A Volume in the Molecular Nutrition SeriesHypothalamic-pituitary-adrenal axis and behavioral dysfunction following early binge-like prenatal alcohol exposure in mice
2015, AlcoholCitation Excerpt :Exemplary are reports describing the impact of PAE on fetal programming of the HPA axis response to stressors (Hellemans, Sliwowska, Verma, & Weinberg, 2010; Kim, Turnbull, Lee, & Rivier, 1999; Ogilvie & Rivier, 1997; Weinberg, Sliwowska, Lan, & Hellemans, 2008; Weinberg, Taylor, & Gianoulakis, 1996). Both rodents (Kim, Giberson, Yu, Zoeller, & Weinberg, 1999; Lee, Imaki, Vale, & Rivier, 1990; Nelson et al., 1986; Taylor, Branch, Liu, & Kokka, 1982; Weinberg, 1992) and primates (Schneider, Moore, Kraemer, Roberts, & DeJesus, 2002) exposed prenatally to alcohol display enhanced HPA axis reactivity to multiple types of stressors, including morphine administration, restraint stress, footshock, cardiac puncture, and cold stress. Furthermore, an overall increase in depression-like symptoms as measured on the forced swim task (Carneiro et al., 2005; Hellemans, Verma, et al., 2010; Wilcoxon, Kuo, Disterhoft, & Redei, 2005) and anxiety-like behavior as measured on the elevated plus maze (Carneiro et al., 2005; Dursun, Jakubowska-Doğru, & Uzbay, 2006; Liang et al., 2014) was found in rats.
Prenatal alcohol exposure: Fetal programming and later life vulnerability to stress, depression and anxiety disorders
2010, Neuroscience and Biobehavioral ReviewsEffects of prenatal ethanol exposure on regulation of basal hypothalamic-pituitary-adrenal activity and hippocampal 5-HT<inf>1A</inf> receptor mRNA levels in female rats across the estrous cycle
2008, PsychoneuroendocrinologyCitation Excerpt :Animals exposed to ethanol in utero show increased HPA activation and/or delayed or deficient recovery to basal levels following stress (Kim et al., 1996; Lee et al., 2000; Nelson et al., 1986; Taylor et al., 1984, 1988; Weinberg, 1988, 1993b). These changes appear to reflect both increased HPA drive and deficits in feedback regulation of HPA activity, and/or an altered balance between drive and feedback (Glavas et al., 2006, 2007; Lee et al., 1990, 2000; Weinberg, 1993b). Importantly, evidence suggests an increased incidence of mental health problems in children and adults with prenatal alcohol exposure, including emotional and psychiatric disorders, and among these, a high incidence of depression and anxiety disorders (Famy et al., 1998; O’Connor and Paley, 2006; Streissguth et al., 1996).
Novel role of adrenergic neurons in the brain stem in mediating the hypothalamic-pituitary axis hyperactivity caused by prenatal alcohol exposure
2008, NeuroscienceCitation Excerpt :In fact, c-fos signals in CRF-ir cells only increased in response to footshock stress as previously shown (Rivest and Rivier, 1994). Likewise, even though our laboratory has previously demonstrated footshock-induced increases of CRF heteronuclear (hn) RNA and mRNA levels in the PVN (Lee et al., 1990; Lee et al., 2000a), our current study did not show any changes in the overall number of CRF-ir neurons. These results may seem conflicting, but it is important to note that changes in hnRNA or mRNA levels do not necessarily translate to observable changes in immunoreactive cell counts.
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Supported by NIH Grants AA06420, DK26741, and HD13527 (C.R.) and a training grant from AA07456 (S.L.), and conducted in part by the Clayton Foundation for Research, California Division. C.R. and W.V. are Clayton Foundation investigators.