Original articleHuman placental norepinephrine transporter mRNA: Expression and correlation with fetal condition at birth
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Transfer of maternal psychosocial stress to the fetus
2020, Neuroscience and Biobehavioral ReviewsAcute psychiatric illness and drug addiction during pregnancy and the puerperium
2020, Handbook of Clinical NeurologyCitation Excerpt :Blocking of norepinephrine and serotonin transporters may increase the concentration of norepinephrine and serotonin 5-hydroxytryptamine (5HT), resulting in narrowing of blood vessels and decrease in blood flow to the placenta (Ramamoorthy et al., 1995). Also, the downregulation of the placental norepinephrine transporter due to amphetamine can result in an increase in circulating catecholamines, downregulation of 11β-hydroxysteroid dehydrogenase-2 (11β-HSD-2), and chronic fetal hypercortisolism, which can cause behavioral problems such as excitement and attention deficit by changing the HPA axis (Bzoskie et al., 1997). The effects of using amphetamine during pregnancy include a higher risk of preeclampsia, preterm birth, more cesarean sections, RCVS, and more maternal morbidity and mortality (Ducros, 2012; Oei et al., 2012).
Passive Addiction and Teratogenic Effects
2018, Volpe's Neurology of the NewbornRole of catecholamines in maternal-fetal stress transfer in sheep
2015, American Journal of Obstetrics and GynecologyCitation Excerpt :Fetal catecholamine homeostasis is maintained through the placental reuptake of neurotransmitters contributing to nearly 50% of the total fetal NE clearance.37 Catecholamine reuptake is achieved by the placental NE transporter,38 which expression is known to be impaired with placental dysfunction or fetal distress.39 Thus, fetal plasma catecholamine concentration is low under physiological conditions though fetal catecholamine production is high compared to postnatal conditions.40
Reconceptualizing in a dual-system model the effects of prenatal cocaine exposure on adolescent development: A short review
2011, International Journal of Developmental NeuroscienceCitation Excerpt :Serving as a barrier to high levels of maternal glucocorticoids, the key enzyme to protect fetal HPA-axis development is placental 11β-HSD-2 (White et al., 1997). Sarkar and colleagues investigated the regulatory mechanism of the 11β-HSD-2 enzyme and found that 11β-HSD-2 gene expression was downregulated by catecholamines, which in turn was affected by maternal cocaine use since the main molecular targets of cocaine binding were catecholamine transporters (Bzoskie et al., 1997; Sarkar et al., 2001). Maternal cocaine use may have deleterious effects on the development of the fetal HPA-axis by weakening protections from the 11β-HSD-2 gene (Lester and Padbury, 2009).
Fetal Effects of Psychoactive Drugs
2009, Clinics in PerinatologyCitation Excerpt :Blockage of these transporters increases the concentrations of norepinephrine and serotonin, resulting in constriction of blood vessels and decreased blood flow to the placenta. Also, placental NET downregulation resulting from MA could lead to increases in circulating catecholamines, downregulation of 11β-HSD-2, and chronic fetal hypercortisolism,28,59 which could affect behavior through alteration of the hypothalamic-pituitary-adrenal axis, especially arousal regulation and attention.43 Each year at least 600,000 infants born in the United States are exposed to maternal major depressive disorder during gestation, which is associated with newborn medical and neurobehavioral deficits and long-term emotional, behavioral, and social problems in the child.