Psychoneuroendocrinology · 2026
Altered placental expression of neurotransmitter and stress-related molecules in first-episode psychosis during pregnancy: Implications for cytoarchitecture and function.
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García-Montero Cielo, Fraile-Martinez Óscar, Boaru Diego Liviu, Castro-Martinez Patricia de, Leon-Oliva Diego De, García-González Beatriz, Pérez-González Isabel, Bravo Coral, Leon-Luis Juan A De, Diaz-Pedrero Raul, Lopez-Gonzalez Laura, Barrena-Blázquez Silvestra, Bujan Julia, García-Honduvilla Natalio, Alvarez-Mon Miguel Ángel, Presa Marta, Lahera Guillermo, Alvarez-Mon Melchor, Saez Miguel A, Ortega Miguel A
Аннотация
BACKGROUND: First-episode psychosis during pregnancy (FEP-PW) is a rare but serious condition that intersects maternal mental health and placental-fetal biology. While psychosis is characterized by disruptions in perception and cognition, its impact on placental neuroendocrine signaling and fetal development remains poorly understood. The placenta, as a key mediator of intrauterine environment, expresses receptors involved in neurotransmission and stress response, potentially linking maternal psychopathology to fetal neurodevelopmental risk.
OBJECTIVE: This study investigates the expression of five critical neuroendocrine and stress-related molecules-dopamine receptor D2 (DRD2), serotonin receptor 1B (HTR1B), glucocorticoid receptor (NR3C1), 11β-hydroxysteroid dehydrogenase type 2 (HSD11B2), and melatonin receptor 1B (MTNR1B)-in placental tissue from women with FEP-PW compared to healthy pregnant controls (HC-PW).
METHODS: Using a prospective case-control design, placental samples from 22 FEP-PW and 20 HC-PW women were analyzed. Gene expression was quantified by real-time quantitative polymerase chain reaction (RT-qPCR), and protein localization and abundance assessed via immunohistochemistry (IHC).
RESULTS: Significant alterations in placental gene and protein expression were observed in FEP-PW placentas: DRD2, NR3C1, and HSD11B2 were markedly upregulated (all p < 0.001 at gene and protein levels), whereas HTR1B and MTNR1B were significantly downregulated compared to controls (p < 0.05, p < 0.01 respectively at gene level and p < 0.01, p < 0.001 at protein level). These findings indicate dysregulated dopaminergic, serotonergic, glucocorticoid, and melatonin signaling pathways in the placenta associated with maternal psychosis.
CONCLUSIONS: Our results provide novel evidence of distinct placental molecular adaptations in FEP-PW, reflecting heightened maternal stress and disrupted neurohormonal environments. These alterations may contribute to adverse placental function and influence fetal neurodevelopmental trajectories, underscoring the placenta's role as a critical mediator in the maternal-placental-fetal axis in psychiatric disorders. Further research is needed to clarify the functional consequences and explore these molecules as potential biomarkers or therapeutic targets in perinatal psychiatry.
OBJECTIVE: This study investigates the expression of five critical neuroendocrine and stress-related molecules-dopamine receptor D2 (DRD2), serotonin receptor 1B (HTR1B), glucocorticoid receptor (NR3C1), 11β-hydroxysteroid dehydrogenase type 2 (HSD11B2), and melatonin receptor 1B (MTNR1B)-in placental tissue from women with FEP-PW compared to healthy pregnant controls (HC-PW).
METHODS: Using a prospective case-control design, placental samples from 22 FEP-PW and 20 HC-PW women were analyzed. Gene expression was quantified by real-time quantitative polymerase chain reaction (RT-qPCR), and protein localization and abundance assessed via immunohistochemistry (IHC).
RESULTS: Significant alterations in placental gene and protein expression were observed in FEP-PW placentas: DRD2, NR3C1, and HSD11B2 were markedly upregulated (all p < 0.001 at gene and protein levels), whereas HTR1B and MTNR1B were significantly downregulated compared to controls (p < 0.05, p < 0.01 respectively at gene level and p < 0.01, p < 0.001 at protein level). These findings indicate dysregulated dopaminergic, serotonergic, glucocorticoid, and melatonin signaling pathways in the placenta associated with maternal psychosis.
CONCLUSIONS: Our results provide novel evidence of distinct placental molecular adaptations in FEP-PW, reflecting heightened maternal stress and disrupted neurohormonal environments. These alterations may contribute to adverse placental function and influence fetal neurodevelopmental trajectories, underscoring the placenta's role as a critical mediator in the maternal-placental-fetal axis in psychiatric disorders. Further research is needed to clarify the functional consequences and explore these molecules as potential biomarkers or therapeutic targets in perinatal psychiatry.