Evidence map›Paper›PMID 31711155›Full record

ReviewBiology of reproduction2020

Placental serotonin signaling, pregnancy outcomes, and regulation of fetal brain development†.

Cheryl S Rosenfeld

Open access · greenAbstract readReview
In one paragraph

Review in Biology of reproduction, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
9.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

69 citing papers in PubMed, 112 citations in OpenAlex.

  1. Article
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  6. Review
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  16. Potential adverse events of fluoxetine: a real-world study based on the FAERS database.Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999) · 2025
    Article
  17. Article
  18. Timing of selective serotonin reuptake inhibitor use and risk for preterm birth and related adverse events: with a consideration of the COVID-19 pandemic period.The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2024
    Article
  19. Article
  20. Article

9 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Cheryl S RosenfeldBond Life Sciences Center, University of Missouri, Columbia, MO USA.
Center for Autism and Related Disorders · US

Funding

Endocrine Disrupting Chemicals, Epigenetic Alterations, and Autism-Like Behaviors in the Highly Social California Mouse ModelR01ES025547 · NIEHS · UNIVERSITY OF MISSOURI-COLUMBIA · PI ROBERTS, R. MICHAEL · 2016 to 2020
$1.9M
NIEHS NIH HHS R01 ES025547
6 · The paper itself

Abstract

The placenta is a transient organ but essential for the survival of all mammalian species by allowing for the exchanges of gasses, nutrients, and waste between maternal and fetal placenta. In rodents and humans with a hemochorial placenta, fetal placenta cells are susceptible to pharmaceutical agents and other compounds, as they are bathed directly in maternal blood. The placenta of mice and humans produce high concentrations of serotonin (5-HT) that can induce autocrine and paracrine effects within this organ. Placental 5-HT is the primary source of this neurotransmitter for fetal brain development. Increasing number of pregnant women at risk of depression are being treated with selective serotonin-reuptake inhibitors (SSRIs) that bind to serotonin transporters (SERT), which prevents 5-HT binding and cellular internalization, allowing for accumulation of extracellular 5-HT available to bind to 5-HT(2A) receptor (5-HT(2A)R). In vitro and in vivo findings with SSRI or pharmacological blockage of the 5-HT(2A)R reveal disruptions of 5-HT signaling within the placenta can affect cell proliferation, division, and invasion. In SERT knockout mice, numerous apoptotic trophoblast cells are observed, as well as extensive pathological changes within the junctional zone. Collective data suggest a fine equilibrium in 5-HT signaling is essential for maintaining normal placental structure and function. Deficiencies in placental 5-HT may also result in neurobehavioral abnormalities. Evidence supporting 5-HT production and signaling within the placenta will be reviewed. We will consider whether placental hyposerotonemia or hyperserotonemia results in similar pathophysiological changes in the placenta and other organs. Lastly, open ended questions and future directions will be explored.

Indexed as

AnimalsBrainEmbryonic DevelopmentFemaleHumansPlacentaPregnancyPregnancy OutcomeSerotoninSignal TransductionSerotonin5-HTanti-depressantsautismgestationgiant cellspre-eclampsiaSERTSSRItrophoblast

Identifiers

PMID31711155
PMCPMC7443348
OpenAlexW2987962964

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.