Amphetamine sensitization and cross-sensitization with acute restraint stress: impact of prenatal alcohol exposure in male and female rats.

Rationale: Individuals with fetal alcohol spectrum disorder (FASD) are at increased risk for substance use disorders (SUD). In typically developing individuals, susceptibility to SUD is associated with alterations in dopamine and hypothalamic-pituitary-adrenal (HPA) systems, and their interactions. Prenatal alcohol exposure (PAE) alters dopamine and HPA systems, yet effects of PAE on dopamine-HPA interactions are unknown.

Prenatal alcohol exposure reduces the proportion of newly produced neurons and glia in the dentate gyrus of the hippocampus in female rats.

Prenatal alcohol exposure (PAE) alters adult neurogenesis and the neurogenic response to stress in male rats. As the effects of stress on neurogenesis are sexually dimorphic, the present study investigated the effects of PAE on adult hippocampal neurogenesis under both nonstressed and stressed conditions in female rats. Pregnant females were assigned to one of three prenatal treatments: (1) alcohol (PAE)-liquid alcohol (ethanol) diet ad libitum (36% ethanol-derived calories); (2) pair-fed-isocaloric liquid diet, with maltose-dextrin substituted for ethanol, in the amount consumed by a PAE partner (g/kg body wt/day of gestation); and (3) control-lab chow ad libitum.

Prenatal alcohol exposure and chronic mild stress differentially alter depressive- and anxiety-like behaviors in male and female offspring.

Background: Fetal Alcohol Spectrum Disorder (FASD) is associated with numerous neurobehavioral alterations, as well as disabilities in a number of domains, including a high incidence of depression and anxiety disorders. Prenatal alcohol exposure (PAE) also alters hypothalamic-pituitary-adrenal (HPA) function, resulting in increased responsiveness to stressors and HPA dysregulation in adulthood. Interestingly, data suggest that pre-existing HPA abnormalities may be a major contributory factor to some forms of depression, particularly when an individual is exposed to stressors later in life.

Effects of prenatal ethanol exposure on basal limbic-hypothalamic-pituitary-adrenal regulation: role of corticosterone.

Background: Rats prenatally exposed to ethanol (E) exhibit hypothalamic-pituitary-adrenal (HPA) hyperresponsiveness and changes in central HPA regulation following exposure to stressors. Whether ethanol-induced alterations in basal HPA regulation play a role in mediating HPA hyperresponsiveness remains unclear. We utilized adrenalectomy (ADX), with or without corticosterone (CORT) replacement, to investigate basal HPA function and the role of CORT in mediating ethanol-induced alterations.

Hypothalamic-pituitary-adrenal responses to 5-HT1A and 5-HT2A/C agonists are differentially altered in female and male rats prenatally exposed to ethanol.

Background: Prenatal ethanol exposure alters the development of the hypothalamic-pituitary-adrenal (HPA) axis, resulting in HPA hyper-responsiveness to stressors in adulthood. Prenatal ethanol exposure also alters the development and activity of the serotoninergic (5-HT) system. We have previously shown that 5-HT(1A) and 5-HT(2A/C) receptor-mediated behavioral and physiological function are altered in fetal ethanol-exposed offspring.

Effects of mineralocorticoid and glucocorticoid receptor blockade on hypothalamic-pituitary-adrenal function in female rats prenatally exposed to ethanol.

Background: Rats prenatally exposed to ethanol (E) exhibit hypothalamic-pituitary-adrenal (HPA) hyperresponsiveness, demonstrated by increased and/or prolonged elevations of adrenocorticotropic hormone (ACTH) and/or corticosterone (CORT) in response to stressors. The present study examined the possible role of CORT feedback deficits in mediating this hyperresponsiveness by examining HPA function following mineralocorticoid (MR) and glucocorticoid (GR) receptor blockade.

Methods: Adult female Sprague-Dawley offspring from E, pair-fed (PF), and control (C) groups were injected subcutaneously with the MR antagonist spironolactone (SPIRO; 30 mg/kg bw), the GR antagonist RU38486 (120 mg/kg bw), or vehicle.

Prenatal ethanol exposure in rats alters serotonergic-mediated behavioral and physiological function.

Rationale: Animals prenatally exposed to ethanol (ethanol-exposed animals) exhibit physiological and behavioral abnormalities consistent with altered 5-hyrdroxytryptamine (5-HT) function including lack of response inhibition and increased anxiety and aggression.

Objective: The present study investigated the possibility that ethanol-exposed animals show alterations in 5-HT(1A) and 5-HT(2A) receptor function, two 5-HT receptor subtypes mediating these behaviors. We measured the physiological and behavioral responses to the 5-HT(1A) agonist 8-hydroxy-2-(di- n-propylamino)tetralin (8-OH-DPAT), and the 5-HT(2A/C)agonist (+/-)-1-(2, 5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride) (DOI), which provide indices for estimating central changes in 5-HT activity and receptor function.