ArticlePsychoneuroendocrinology2016
A pharmacological mouse model suggests a novel risk pathway for postpartum psychosis.
Article in Psychoneuroendocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- Does hypothalamic CCN3 hypersecretion confer postpartum mood disorder risk?Translational psychiatry · 2026Review
- Cardiac arrhythmia, developmental delay, epilepsy and ichthyosis due to Xp22.31 deletion: review of literature and case report.Translational pediatrics · 2025Article
- Postpartum Psychosis: A Review of Risk Factors, Clinical Picture, Management, Prevention, and Psychosocial Determinants.Medical science monitor : international medical journal of experimental and clinical research · 2023Review
- X-linked ichthyosis: New insights into a multi-system disorder.Skin health and disease · 2022Review
- Comorbid Medical Issues in X-Linked Ichthyosis.JID innovations : skin science from molecules to population health · 2022Article
- Behavioural and molecular characterisation of the Dlg2 haploinsufficiency rat model of genetic risk for psychiatric disorder.Genes, brain, and behavior · 2022Article
- The role of the immune system in postpartum psychosis.Brain, behavior, & immunity - health · 2021Article
- A new molecular risk pathway for postpartum mood disorders: clues from steroid sulfatase-deficient individuals.Archives of women's mental health · 2021Review
- Immune System Alterations and Postpartum Mental Illness: Evidence From Basic and Clinical Research.Frontiers in global women's health · 2021Review
- Medical and neurobehavioural phenotypes in carriers of X-linked ichthyosis-associated genetic deletions in the UK Biobank.Journal of medical genetics · 2020Article
- An Analysis of Cellular Communication Network Factor Proteins as Candidate Mediators of Postpartum Psychosis Risk.Frontiers in psychiatry · 2019Article
- Brain Gene Expression in a Novel Mouse Model of Postpartum Mood Disorder.Translational neuroscience · 2019Article
- Behavioural and psychiatric phenotypes in female carriers of genetic mutations associated with X-linked ichthyosis.PloS one · 2019Article
- Do Defective Immune System-Mediated Myelination Processes Increase Postpartum Psychosis Risk?Trends in molecular medicine · 2018Review
- X-linked ichthyosis associated with psychosis and behavioral abnormalities: a case report.Journal of medical case reports · 2017Article
- Understanding the pathophysiology of postpartum psychosis: Challenges and new approaches.World journal of psychiatry · 2017Review
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Postpartum psychosis (PP) is a severe psychiatric disorder affecting a small proportion of new mothers shortly after childbirth. The molecular pathophysiology underlying the disorder is currently poorly understood, and there are no amenable animal models for the condition; maternal deficiency for the enzyme steroid sulfatase has been proposed as a potential risk mechanism. Here we show that inhibition of steroid sulfatase with 667-COUMATE (10mg/kg p.o.) in new mouse mothers results in behavioural abnormalities that can be partially alleviated by the administration of the clinically-efficacious antipsychotic ziprasidone (0.3-1.0mg/kg i.p.). The pattern of behavioural abnormalities in 667-COUMATE-treated mice implicated a genetic substrate at 21-23cM on chromosome 15; of the 17 genes within this chromosomal interval, only one (Nov/Ccn3) was significantly differentially expressed in the brains of vehicle and 667-COUMATE-treated mice. Two additional members of the Ccn family (Ccn2/Ctgf and Ccn4/Wisp1) were also significantly differentially expressed between the two groups, as were three further genes co-expressed with Nov/Ccn3 in brain (Arhgdig) or previously implicated in disorder risk by clinical studies (Adcy8 and Ccl2). The expression of Nov/Ccn3, but not of the other differentially-expressed genes, could be normalised by ziprasidone administration (1.0mg/kg). NOV/CCN3 lies directly under a linkage peak for PP risk at 8q24, and the associated protein possesses numerous characteristics that make it an excellent candidate mediator of PP risk. Our data suggest the 667-COUMATE-treated mouse as a model for PP with some degree of face, construct, and predictive validity, and implicate a novel, and biologically-plausible, molecular risk pathway for PP.
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Registered trials
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.