Postnatal handling does not normalize hypothalamic corticotropin-releasing factor mRNA levels in animals prenatally exposed to ethanol

Prenatal alcohol exposure and cortisol activity in 19-month-old toddlers: an investigation of the moderating effects of sex and testosterone

“…Sex-specific patterns of associations between PAE and social behaviors, brain structures, and neuroendocrine activity are commonly reported in animal studies (Kelly et al 2000). Higher responses to unfamiliar situations shown in UPAE males, but not in UPAE females, are in agreement with previous findings reporting higher LHPA responses to prolonged/repeated stressors in PAE male rodents (Gabriel et al 2005;Weinberg et al 2008). Notably, previous studies investigating the effects of PAE on stress-related systems does not suggest pervasive increases in all neuroendocrine markers of stress, but rather indicate changes in specific components of the stress response, which may affect differently males and females (Kelly and Dillingham 1994).…”

“…Higher glucocorticoid responses to acute/short duration stressors (e.g., restraint) are more often reported in PAE females, although PAE males show higher responses to prolonged or repeated stressors (for a review, see Weinberg et al 2008). For example, postnatal handling was associated with higher basal hypothalamic CRH mRNA in PAE males, but not in PAE females (Gabriel et al 2005).…”

“…More specifically, we hypothesized that PAE toddlers would show enhanced pretest and cortisol responses to unfamiliar situations compared to nonexposed children. Based on previous rodent studies (Gabriel et al 2005;Weinberg et al 2008), we further hypothesized that the associations between PAE and cortisol responses to our stressful paradigm would be stronger for boys than for girls. Finally, we explored the possibility that testosterone moderated the association between PAE and cortisol activity.…”

Effects of Mineralocorticoid and Glucocorticoid Receptor Blockade on Hypothalamic–Pituitary–Adrenal Function in Female Rats Prenatally Exposed to Ethanol

“…For example, in response to stressors, such as footshock and endotoxemia, Lee et al (2000) demonstrated that ethanol-exposed offspring exhibit enhanced immediate early gene (c-fos and NGFI-B) and corticotropin-releasing hormone (CRH) heteronuclear RNA responses compared with C offspring, providing the first evidence that HPA hyperresponsiveness may be mediated by enhanced stimulatory inputs to the paraventricular nucleus (PVN). Our recent data demonstrating that, under basal conditions, adult E males and females exhibit elevated basal PVN CRH mRNA levels (Gabriel et al, 2005) as well as greater ADX-induced elevations of CRH mRNA (Zhang et al, 2005) than their C counterparts, support and extend these findings suggesting enhanced drive to the PVN under basal conditions, even in the face of similar basal hormone levels.…”

Aniracetam Reversed Learning and Memory Deficits Following Prenatal Ethanol Exposure by Modulating Functions of Synaptic AMPA Receptors

“…Experimental models of FASD have shown cognitive deficits at all ages, from pre-weaning life through late adulthood (Barr et al, 2005). Deficits have been observed in a wide variety of learning and memory tasks, including spatial reference memory (Gabriel et al, 2005;Kim et al, 1997;Matthews and Simson, 1998;Zimmerberg and Weston, 2002), working memory (Neese et al, 2004), and associative memory (Clausing et al, 1995;Vaglenova, 1992;Vaglenova andPetkov, 1998, 2001;Weeber et al, 2001).…”