Objective We sought to determine if maternal depression, anxiety, and/or treatment with selective serotonin reuptake inhibitors (SSRIs) affect placental human serotonin transporter (SLC6A4), norepinephrine transporter (SLC6A2), and 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) gene expression. Methods Relative mRNA expression was compared among placental samples (n=164) from healthy women, women with untreated depression and/or anxiety symptoms during pregnancy, and women who used SSRIs. Results SLC6A4 expression was significantly increased in placentas from women with untreated mood disorders and from women treated with SSRIs, compared to controls. SLC6A2 and 11β-HSD2 expression was increased in non-control groups, though the differences were not significant. SLC6A4, SLC6A2, and 11β-HSD2 expression levels were positively correlated. Conclusions The finding that maternal depression/anxiety affects gene expression of placental SLC6A4 suggests a possible mechanism for the effect(s) of maternal mood on fetal neurodevelopmental programming. SSRI treatment does not further alter the elevated SLC6A4 expression levels observed with exposure to maternal depression or anxiety.
There has been a longstanding concern with the fetal effects of psychoactive drug use by pregnant women. In this article we describe the effects of three drugs with similar molecular targets that involve monoaminergic transmitter systems. These stimulants include the illegal drugs cocaine and methamphetamine and the class of selective serotonin re-uptake inhibitors (SSRIs) used to treat maternal depression during pregnancy. We discuss the mechanisms of action of each drug, including a possible common epigenetic mechanism for their effects on the developing child. We also discuss fetal neurobehavioral techniques that may be useful in the early detection of the effects of in utero drug exposure.In the past three decades, the concept of behavioral teratology 1 expanded the field of teratology to examine behavioral effects in the neonate due to acute exposure to substances in utero, including environmental, nutritional, and drug exposures. 2,3 The developmental consequences of prenatal exposure to a toxic substance may include central nervous system (CNS) insult related to the period during gestation of the exposure. In contrast to the effects of drugs on the adult brain, which result in deformation of the developed brain, fetal effects are more likely to produce malformation in which the developing brain is prevented from forming normally. 4 The effects of exposure during the first half of gestation will impact processes related to cytogenesis and histogenesis whereas effects during the second half of gestation relate to brain growth and differentiation. During this organizational phase in the second half of gestation, progressive events (neuroblast proliferation and migration, axonal projection, and Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Recent years have seen further expansion of the principles of behavioral teratology to examine exposure effects on the human fetus at the time of the exposure. Epigenetic and organismic models of developmental theory suggest that true understanding of a developing system can occur with the study of its organization of form and structure as it moves toward a teleological state. 5,6 This study includes examination of the mutual influences of genes, physiology, and behavior as well as the physical, cultural, and social environments of the organism. 6 NIH Public AccessIncreasing evidence from preclinical, prospective clinical and epidemiological studies suggests that many biological factors acting during prenatal life are associated with adult disease as well as long term neurobehavioral abnormalities 7-17 and behavioral disorders. [18...
We examined the contribution of the fetal membranes, amnion and chorion, to human embryonic and fetal hematopoiesis. A population of cells displaying a hematopoietic progenitor phenotype (CD34 ++ CD45 low ) of fetal origin was present in the chorion at all gestational ages, associated with stromal cells or near blood vessels, but was absent in the amnion. Prior to 15 weeks of gestation, these cells lacked hematopoietic in vivo engraftment potential. Differences in the chemokine receptor and β1 integrin expression profiles of progenitors between the first and second trimesters suggest that these cells had gestationally regulated responses to homing signals and/or adhesion mechanisms that influenced their ability to colonize the stem cell niche. Definitive hematopoietic stem cells, capable of multilineage and long-term reconstitution when transplanted in immunodeficient mice, were present in the chorion from 15-24 weeks gestation, but were absent at term. The second trimester cells also engrafted secondary recipients in serial transplantation experiments. Thus, the human chorion contains functionally mature hematopoietic stem cells at mid-gestation.
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