The relationship between adult health and childhood maltreatment, as moderated by anger and ethnic background.

Childhood maltreatment, anger, and racial/ethnic background were examined in relation to physical health, psychological well-being, and blood pressure outcomes. This study used data from a diverse sample of African American, Latino, and Caucasian participants (N=198). Results from a series of multiple regressions indicated anger and total childhood maltreatment were robust predictors of poorer health.

Mid- to late gestational morphine exposure does not alter the rewarding properties of morphine in adult male rats.

Prenatal exposure to drugs of abuse often leads to physiological and neurobiological abnormalities including decreased brain and body weight, cognitive deficits and behavioral alterations. A handful of studies showed increased vulnerability to drug abuse in prenatally drug-exposed offspring. Our work also demonstrated that prenatal exposure to analgesic doses of morphine during gestation days 11-18 increases mu-opioid receptor density in the nucleus accumbens and central amygdala of adult male rats.

Hypothalamo-pituitary-adrenal axis-regulated stress response and negative feedback sensitivity is altered by prenatal morphine exposure in adult female rats.

It has been shown that adult female rats react to stressors more intensely than adult male rats. Our previous work demonstrated that the adrenocorticotropic hormone (ACTH) but not corticosterone (CORT) response to stress is altered by prenatal morphine exposure in adult male rats. Response of the hypothalamo-pituitary-adrenal (HPA) axis to stress is known to be sex specific and dependent on the hormonal fluctuation of the estrous cycle.

Adrenocorticotropin stress response but not glucocorticoid-negative feedback is altered by prenatal morphine exposure in adult male rats.

The present study was designed to investigate the effects of prenatal morphine exposure on the hypothalamic-pituitary-adrenal (HPA) axis-regulated stress responses by measuring restraint stress-induced changes in the adrenocorticotropic hormone (ACTH) and corticosterone (CORT) levels. In experiment 1, plasma levels of ACTH and CORT in prenatally morphine-, saline-exposed and control male rats were determined before and at several times after restraint stress. There were no statistically significant differences in plasma ACTH and CORT levels before restraint stress between the groups.

Autoradiographic evidence that prenatal morphine exposure sex-dependently alters mu-opioid receptor densities in brain regions that are involved in the control of drug abuse and other motivated behaviors.

The present study examined the effects of prenatal morphine exposure on mu-opioid receptor density in young adult male and female rats to assess the long-term alterations in several brain areas including the nucleus accumbens (NAc), bed nucleus of stria terminalis (BNST), and the basolateral (BLA), lateral (LA), central (CeA), and posteromedial cortical (PMCoA) amygdaloid nuclei. These brain areas are involved in motivating and rewarding behaviors of opiates and other drugs of abuse. The reinforcing actions of opiates appear to be mu-opioid receptor dependent.

Mu-opioid receptors in seizure-controlling brain structures are altered by prenatal morphine exposure and by male and female gonadal steroids in adult rats.

The present study used autoradiography to examine the effect of prenatal morphine exposure on mu-opioid receptor density in epileptic seizure-controlling brain structures including the substantia nigra pars compacta (SNC), substantia nigra pars reticulata (SNR), superior colliculus (SC), and subthalamic nucleus (STN) of adult male and female rats. The results demonstrate that prenatal morphine exposure increases the mu-opioid receptor density in the SNC and STN, but not in the SNR or in the SC of gonadally intact adult male rats. The density of mu-opioid receptors in the SNC and STN is, however, decreased following gonadectomy in morphine-exposed males, and testosterone treatment fails to restore this decrease to the level of gonadally intact males.