ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2012
Altered serotonergic function may partially account for behavioral endophenotypes in steroid sulfatase-deficient mice.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- Physiological and Behavioural Characterisation of a Novel Steroid Sulfatase-Deficient Mouse.Genes, brain, and behavior · 2026Article
- Memory, mood and associated neuroanatomy in individuals with steroid sulphatase deficiency (X-linked ichthyosis).Genes, brain, and behavior · 2024Article
- An updated review on animal models to study attention-deficit hyperactivity disorder.Translational psychiatry · 2024Review
- Estrogen sulfotransferase and sulfatase in steroid homeostasis, metabolic disease, and cancer.Steroids · 2024Review
- Xp22.31 copy number variations in 87 fetuses: refined genotype-phenotype correlations by prenatal and postnatal follow-up.BMC medical genomics · 2023Article
- X-linked ichthyosis: New insights into a multi-system disorder.Skin health and disease · 2022Review
- Steroid Sulfation in Neurodegenerative Diseases.Frontiers in molecular biosciences · 2022Review
- A new molecular risk pathway for postpartum mood disorders: clues from steroid sulfatase-deficient individuals.Archives of women's mental health · 2021Review
- Medical and neurobehavioural phenotypes in male and female carriers of Xp22.31 duplications in the UK Biobank.Human molecular genetics · 2020Article
- Medical and neurobehavioural phenotypes in carriers of X-linked ichthyosis-associated genetic deletions in the UK Biobank.Journal of medical genetics · 2020Article
- 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
- Exploring the Validity of Proposed Transgenic Animal Models of Attention-Deficit Hyperactivity Disorder (ADHD).Molecular neurobiology · 2018Review
- Understanding the pathophysiology of postpartum psychosis: Challenges and new approaches.World journal of psychiatry · 2017Review
- A pharmacological mouse model suggests a novel risk pathway for postpartum psychosis.Psychoneuroendocrinology · 2016Article
- Behavioural and Psychiatric Phenotypes in Men and Boys with X-Linked Ichthyosis: Evidence from a Worldwide Online Survey.PloS one · 2016Article
- Motivational assessment of mice using the touchscreen operant testing system: effects of dopaminergic drugs.Psychopharmacology · 2015Article
- Aberrant Monoaminergic System in Thyroid Hormone Receptor-β Deficient Mice as a Model of Attention-Deficit/Hyperactivity Disorder.The international journal of neuropsychopharmacology · 2015Article
- Genetic and pharmacological modulation of the steroid sulfatase axis improves response control; comparison with drugs used in ADHD.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014Article
- Altered brain gene expression but not steroid biochemistry in a genetic mouse model of neurodevelopmental disorder.Molecular autism · 2014Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The X-linked gene STS encodes the steroid hormone-modulating enzyme steroid sulfatase. Loss-of-function of STS, and variation within the gene, have been associated with vulnerability to developing attention deficit hyperactivity disorder (ADHD), a neurodevelopmental condition characterized by inattention, severe impulsivity, hyperactivity, and motivational deficits. ADHD is commonly comorbid with a variety of disorders, including obsessive-compulsive disorder. The neurobiological role of steroid sulfatase, and therefore its potential role in ADHD and associated comorbidities, is currently poorly understood. The 39,X(Y)*O mouse, which lacks the Sts gene, exhibits several behavioral abnormalities relevant to ADHD including inattention and hyperactivity. Here, we show that, unexpectedly, 39,X(Y)*O mice achieve higher ratios than wild-type mice on a progressive ratio (PR) task thought to index motivation, but that there is no difference between the two groups on a behavioral task thought to index compulsivity (marble burying). High performance liquid chromatography analysis of monoamine levels in wild type and 39,X(Y)*O brain tissue regions (the frontal cortex, striatum, thalamus, hippocampus, and cerebellum) revealed significantly higher levels of 5-hydroxytryptamine (5-HT) in the striatum and hippocampus of 39,X(Y)*O mice. Significant correlations between hippocampal 5-HT levels and PR performance, and between striatal 5-HT levels and locomotor activity strongly implicate regionally-specific perturbations of the 5-HT system as a neurobiological candidate for behavioral differences between 40,XY and 39,X(Y)*O mice. These data suggest that inactivating mutations and functional variants within STS might exert their influence on ADHD vulnerability, and disorder endophenotypes through modulation of the serotonergic system.
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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.