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.

Prenatal ethanol exposure: sex differences in anxiety and anxiolytic response to a 5-HT1A agonist.

This study utilized a novelty-induced suppression of feeding task to examine anxiety-like behaviour and the anxiolytic effects of the 5-HT1A agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), in rats prenatally exposed to ethanol. Adult offspring from ethanol exposed (E), pair-fed control (PF) and ad libitum-fed control (C) dams were habituated to a novel palatable food for 21 days and measures of baseline feeding obtained. On day 22 (d 22), animals received either 8-OH-DPAT (0.

Prenatal ethanol exposure in rats decreases levels of complexin proteins in the frontal cortex.

Background: Rodents that are prenatally exposed to ethanol have been shown to exhibit a wide range of cognitive deficits, including impairments in memory, attention and executive function. To determine a potential molecular substrate for cognitive dysfunction in adulthood, we measured regional levels of the presynaptic proteins complexin I and II in a rat model of prenatal ethanol exposure, as levels of these proteins are altered in cognitive-related synaptic plasticity.

Methods: Pregnant female rats received either a liquid ethanol diet (36% ethanol-derived calories) or a liquid control diet (maltose-dextrin isocalorically substituted for ethanol, matched in amount [g/kg body wt/day of gestation] to an ethanol-consuming partner), or were given ad libitum-fed access to standard laboratory chow and water.

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.

Exposure to repeated, intermittent d-amphetamine induces sensitization of HPA axis to a subsequent stressor.

Previous studies have demonstrated that exposure to psychostimulant drugs can produce a lasting cross-sensitization to the behavioral effects of stress. The main purpose the present study was, therefore, to determine the effects of psychostimulant cross-sensitization on the stress-induced release of adrenocorticotropic hormone (ACTH) and corticosterone (CORT). Rats were given a series of injections of d-amphetamine or vehicle in a regimen that has been shown previously to induce cross-sensitization to a stressor.