Stress in pregnant rats alters the pattern of secretion of corticosterone (COR) and modifies transplacentally hypothalamic-pituitary-adrenal axis (HPA) fetus. Prenatal stress during the critical hypothalamic differentiation is related to decreased fertility of male offspring by an increase in the basal level of COR. This modification could induce long-term changes in the process of apoptosis in the testis. However, early postnatal handling increases maternal behavior and could reverse the effects caused by increased secretion of COR. The aim of this research was to investigate the effects of early postnatal stimulation of male rats prenatal stressed by chronic immobilization during the last two weeks of pregnancy, on the hypothalamic-pituitary-gonadal axis and their relationship with the activity of the HPA. Male Wistar rats 3 month olds, were separated in four groups: (a) prenatally stressed animals by immobilization (IMO), without postnatal stimulation; (b) prenatally stressed animals with postnatal stimulation; (c) control animals without prenatal stress, without postnatal stimulation and (d) control animals without prenatal stress, with postnatal stimulation. In different animals groups plasmatic levels of COR, Testosterone (T) and Luteinizing Hormone (LH) were analyzed. Gonadosomatic index and testicular apoptosis was determined. In conclusion that prenatal stress by IMO increased levels of COR and inhibits the HHG axis obtaining low values of plasmatic LH and T, testicular weight, and induction of apoptosis in testes. On other hand, early postnatal stimulation results in an increase in maternal care to the offspring reversing the effects of prenatal stress on the HPG axis. This effect could be mediated by a mechanism independent of the HPA axis.

Stress in pregnant rats caused by chronic immobilization alters the pattern of secretion of corticosterone and modifies the hypothalamic-pituitary-adrenal axis (HPA) of the fetus. Early postnatal handling, however, may reverse the effects of increased secretion of corticosterone. We investigated the effects of prenatal stress and postnatal handling on the activity of the HPA axis of male offspring of stressed female rats. Male 90-day-old rats from four groups were investigated: prenatally stressed animals without postnatal handling, prenatally stressed animals with postnatal handling, unstressed control animals with postnatal handling, and unstressed control animals without postnatal handling. After sacrifice, the adrenal glands were weighed to determine the adrenal-somatic index. Apoptosis was evaluated by TUNEL assay and active caspase-3 expression. We found that the adrenal gland cortex:medulla ratio increased in animals with prenatal stress and that eventually the stress caused apoptosis. Handling newborns to simulate maternal activity ameliorated some of the negative effects of prenatal stress.

SUMMARY:Chronic stress by immobilization during pregnancy may cause alterations in mechanisms maintaining homeostasis in the adrenal gland. The objective of this study was to quantify cellular proliferation index in the adrenal cortex during pregnancy second half and assess the effects of chronic stress on it. Adrenal cortex proliferation index in stressed rats showed a significant decrease at 12 and 17 days of gestation, while at day 21 it did not show differences with the control treatments. Moreover, proliferation index of reticular zones in control and experimental rats, exhibited a significant reduction in comparison to glomerular and fascicular zones of adrenal cortex during the three gestation days studied. In conclusion, chronic stress by immobilization produces a decrease in cellular proliferation index at 12 and 17 gestation days, which may be related to changes in plasmatic concentrations of corticosterone and prolactin and, to the reduction of specific growth factors. Furthermore, the observed proliferation diminishment in reticular zone regarding the other cortical zones would be consistent with the migration theory of adrenal cells.

The model of chronic intermittent stress by immobilization during pregnancy may produce alterations in the mechanisms that maintain adrenal gland homeostasis. In earlier investigations using this model, significant variations in plasma prolactin and corticosterone levels, and adrenal gland weights were observed. We hypothesized that chronic stress causes changes in apoptosis in the adrenal glands of pregnant rats. We identified and quantified apoptotic cells in the adrenal cortex and examined their ultrastructural characteristics using transmission electron microscopy. Adrenal glands of pregnant rats at gestation days 12, 17 and 21 were studied for control and experimental (stressed) rats. Immunolabelling techniques, stereological analysis and image quantification of adrenal gland sections were combined to determine differences in apoptosis in the different cell populations of the adrenal cortex. The apoptotic index of the experimental rats showed a significant reduction at gestation day 17, while at days 12 and 21 there were no differences from controls. Moreover, the apoptotic index of the reticular zones in control and experimental animals showed a significant increase compared to the glomerular and fascicular zones at the three gestation times studied. Chronic stress by immobilization reduced the caspase-dependent apoptotic index at gestation day 17, which may be related to variations in plasma concentrations of estrogens and prolactin.

No abstract