Maternal stress modifies fetal programming of neuroendocrine development and behavior. These effects are mediated by maternal and fetal corticosteroids and opioids. We evaluated an ability of pharmacological prevention of long-term behavioral and hypothalamicpituitaryadrenal (HPA) disorders in adult rat offspring induced by daily 1 h maternal immobilization during the last gestational week. Dexamethasone (Dex; 0.1 mg/kg per day) or naltrexone (Ntx; 10 mg/kg per day) treatments prior to pregnant rats stressing prevented impairment of copulatory behavior (increase of mounting latency, decrease of ejaculatory rates etc.) in adult male offspring. Both Dex and Ntx exerted protective effect with regard to diminishing adrenocortical and hypothalamic nordarenaline responses to an acute stress as well as decrease of stress-induced activation of GABAA and GABAB receptors tested with muscimol and baclofen in those animals. In prenatally stressed female rats, Ntx prevented enhancement of adrenocortical response to an acute sress while no protective effect of Dex has been found. One of the long-term consequences of prenatal stress was an impairment of adrenocortical response to noradrenaline infusion into the third brain ventricle: it was significantly diminished in females and increased in males. These changes were not observed both in males and females treated prenatally with Dex or Ntx. We concluded that Dex blockade of endocrine response to stress or Ntx blockade of opioid receptors can prevent pathological changes in sexual behavior and HPA noradrenergic and stress reactivity in prenatally stressed rats in gender-related manner.
03 - 07 May 2008
European Society of Endocrinology