Prenatal depression and stress - risk factors for placental pathology and spontaneous abortion.

Prenatal stress and depression affects 10-25% of pregnant women and is associated with disruption of fetal neurodevelopment, higher rates of placental abnormalities, preeclampsia, spontaneous abortion, or preterm birth. Markers of genetic vulnerability are catechol-O-methyltransferase, monoamine oxidase-A, variation of serotonin transporters, low levels of dopamine-beta-hydroxylase, and brain derived neurotrophic factor Val66Met (BDNF), while hyperactivity of HPA (hypothalamic-pituitary-adrenal) axis and massive release of endogenous cortisol, regulated by metalloproteinase-1, -2, -3 and -9, and are involved both in depressive symptoms and neurodevelopmental abnormalities in fetus. In women with prenatal stress and depression which suffered spontaneous abortion were observed placental abnormalities as regular shape and necrotic villi, decidua with large areas of necrosis, acute inflammation and effusion areas correlated with increase in proinflammatory factors, immune deficit and infections, hyaline type fibrosis, intervilos and deciduous intense hemorrhage, associated with increase of vascular endothelial growth factor. Taking into account the important societal and economic costs becomes important for an interdisciplinary approach, in which pregnancy and its risks are a central point for women mental health.

Comparative study of neuroprotective effect of tricyclics vs. trazodone on animal model of depressive disorder.

The neurobiological model of depressive disorder may be correlated with the animal model on rat, hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis, the increase of cortisol level being specific to the model of depression in women. The neurobiological model of depression in women presents vulnerabilities for some cerebral structures (hippocampus, frontal cortex, cerebral amygdala). A decrease of frontal cortex and hippocampus volumes are recognized in depressive disorder in women, depending on duration of disease and antidepressant therapy. Neurobiological vulnerability may be pronounced through cholinergic blockade. The purpose of the study was to highlight the cytoarchitectural changes in the frontal cortex and hippocampus by comparing two antidepressant substances: amitriptyline with a strong anticholinergic effect and trazodone, without anticholinergic effect. The superior neuroprotective qualities of trazodone for the frontal cortex, hippocampus and dentate gyrus are revealed. The particular neurobiological vulnerability of depression in women requires a differentiated therapeutic approach, avoiding the use of antidepressants with anticholinergic action.