ArticleDevelopmental neuroscience2016
Restraint Stress during Pregnancy Rapidly Raises Kynurenic Acid Levels in Mouse Placenta and Fetal Brain.
Article in Developmental neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 63 citations in OpenAlex.
- The placental tryptophan pathway across gestation: implications for pregnancy outcomes.Human reproduction update · 2026Review
- Biochemical Regulation of Brain Kynurenic Acid Synthesis and Inhibition in Rats Is Sensitive to the Time of Day.ACS chemical neuroscience · 2026Article
- Metabolic reprogramming in placenta and umbilical cord serum of polycystic ovary syndrome pregnancies: testosterone-associated alterations and interaction with obesity.Human reproduction open · 2026Article
- Neurochemical Insights into the Role of Tryptophan Metabolites and Kynurenine Pathway in Insomnia and its Psychological and Neurological Comorbidities.Molecular neurobiology · 2025Review
- Understanding How Mental Health Influences IBD Outcomes: A Review of Potential Culprit Biological Mechanisms.Biomedicines · 2025Review
- Functional Impairments in Learning and Signal Propagation Following Prenatal Kynurenine Treatment in Mice.The European journal of neuroscience · 2025Article
- Impact of terminal ileal microbiota dysbiosis and tryptophan metabolism alterations on mental disorders in patients with Crohn's disease.BMC gastroenterology · 2025Article
- Neuroactive Kynurenines as Pharmacological Targets: New Experimental Tools and Exciting Therapeutic Opportunities.Pharmacological reviews · 2024Review
- The Biology and Biochemistry of Kynurenic Acid, a Potential Nutraceutical with Multiple Biological Effects.International journal of molecular sciences · 2024Review
- Fetal Sex as Moderating Factor for the Relationship Between Maternal Childhood Trauma and Salivary Kynurenic Acid and Tryptophan in Pregnancy: A Pilot Study.International journal of tryptophan research : IJTR · 2024Article
- LC-MS/MS-based quantification of tryptophan, kynurenine, and kynurenic acid in human placental, fetal membranes, and umbilical cord samples.Scientific reports · 2023Article
- The stress of losing sleep: Sex-specific neurobiological outcomes.Neurobiology of stress · 2023Article
- A unified model of the biology of peripartum depression.Translational psychiatry · 2023Review
- Review
- Brain Damage in Preterm and Full-Term Neonates: Serum Biomarkers for the Early Diagnosis and Intervention.Antioxidants (Basel, Switzerland) · 2023Review
- Perspective: Gestational Tryptophan Fluctuation Altering Neuroembryogenesis and Psychosocial Development.Cells · 2022Article
- Maternal inflammation and its ramifications on fetal neurodevelopment.Trends in immunology · 2022Review
- Prenatal inflammation as a link between placental expression signature of tryptophan metabolism and preterm birth.Human molecular genetics · 2021Article
- Prenatal stress-induced disruptions in microbial and host tryptophan metabolism and transport.Behavioural brain research · 2021Article
- FOXO1 Is a Critical Switch Molecule for Autophagy and Apoptosis of Sow Endometrial Epithelial Cells Caused by Oxidative Stress.Oxidative medicine and cellular longevity · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Stressful events during pregnancy adversely affect brain development and may increase the risk of psychiatric disorders later in life. Early changes in the kynurenine (KYN) pathway (KP) of tryptophan (TRP) degradation, which contains several neuroactive metabolites, including kynurenic acid (KYNA), 3-hydroxykynurenine (3-HK), and quinolinic acid (QUIN), may constitute a molecular link between prenatal stress and delayed pathological consequences. To begin testing this hypothesis experimentally, we examined the effects of a 2-h restraint stress on KP metabolism in pregnant FVB/N mice on gestational day 17. TRP, KYN, KYNA, 3-HK, and QUIN levels were measured in maternal and fetal plasma and brain, as well as in the placenta, immediately after stress termination and 2 h later. In the same animals, we determined the activity of TRP 2,3-dioxygenase (TDO) in the maternal liver and in the placenta. Compared to unstressed controls, mostly transient changes in KP metabolism were observed in all of the tissues examined. Specifically, stress caused significant elevations of KYNA levels in the maternal plasma, placenta, and fetal brain, and also resulted in increased levels of TRP and KYN in the placenta, fetal plasma, and fetal brain. In contrast, 3-HK and QUIN levels remained unchanged from control values in all tissues at any time point. In the maternal liver, TDO activity was increased 2 h after stress cessation. Taken together, these findings indicate that an acute stress during the late gestational period preferentially affects the KYNA branch of KP metabolism in the fetal brain. Possible long-term consequences for postnatal brain development and pathology remain to be examined.
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