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Prenatal paroxetine dysregulates monoamine homeostasis and affects placental hemodynamics in the rat fetoplacental unit

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11160%2F25%3A10505094" target="_blank" >RIV/00216208:11160/25:10505094 - isvavai.cz</a>

  • Result on the web

    <a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=EC64Ddrh.c" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=EC64Ddrh.c</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.biopha.2025.118680" target="_blank" >10.1016/j.biopha.2025.118680</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Prenatal paroxetine dysregulates monoamine homeostasis and affects placental hemodynamics in the rat fetoplacental unit

  • Original language description

    Antidepressant use during pregnancy is increasingly common, with selective serotonin reuptake inhibitors (SSRIs) widely prescribed for maternal depression. However, growing evidence links prenatal SSRI exposure to adverse outcomes, including impaired placental functions, disrupted fetal development, and long-term neurobehavioral risks. Monoamines such as serotonin, dopamine, and norepinephrine are critical regulators of placental vascular tone, fetal programming, and neurodevelopment, making them highly susceptible to pharmacological disruption. Here, we investigated the effects of prenatal paroxetine on monoamine regulation, metabolite profiles, and fetoplacental hemodynamics in a pregnant rat model. Paroxetine was administered orally at two doses, 15 mg/kg (n = 10) or 50 mg/kg (n = 7) and compared to controls (n = 6). Gene expression of monoamine-related transporters and enzymes was quantified in placenta and fetal brain by qRT-PCR. Placental and fetal brain metabolomes were assessed via LC-MS, and Doppler ultrasound was used to evaluate uterine and fetal vascular parameters. At 15 mg/kg, paroxetine reduced fetal (2.03 +- 1.10 g vs. 2.27 +- 0.92 g) and placental weights (0.35 +- 0.08 g vs. 0.46 +- 0.05 g), downregulated placental expression of serotonin, dopamine, and norepinephrine transporters, disrupted tryptophan metabolism, and increased vascular resistance in umbilical arteries (2.10 +- 0.21 vs. 1.85 +- 0.05). Surprisingly, the 50 mg/kg dose attenuated many of these effects, suggesting non-linear pharmacological response, potentially due to transporter saturation and/or receptor desensitization. Importantly, gene expression and hemodynamic effects were consistent across sexes. These findings provide novel mechanistic insights into the impact of SSRIs on placental function and fetal development, underscoring the complexity of their pharmacokinetics and pharmacodynamics during pregnancy and emphasizing the need for careful dose consideration during pregnancy.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30104 - Pharmacology and pharmacy

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2025

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Biomedicine &amp; Pharmacotherapy

  • ISSN

    0753-3322

  • e-ISSN

    1950-6007

  • Volume of the periodical

    192

  • Issue of the periodical within the volume

    November

  • Country of publishing house

    FR - FRANCE

  • Number of pages

    11

  • Pages from-to

    118680

  • UT code for WoS article

    999

  • EID of the result in the Scopus database

    2-s2.0-105020878919