ArticleEndocrinology2013
The androgen metabolite, 5α-androstane-3β,17β-diol (3β-diol), activates the oxytocin promoter through an estrogen receptor-β pathway.
Article in Endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- Neuroendocrine contribution to sex-related variations in adverse air pollution health effects.Journal of toxicology and environmental health. Part B, Critical reviews · 2024Review
- Giftedness and atypical sexual differentiation: enhanced perceptual functioning through estrogen deficiency instead of androgen excess.Frontiers in endocrinology · 2024Review
- Estradiol and 3β-diol protect female cortical astrocytes by regulating connexin 43 Gap Junctions.Molecular and cellular endocrinology · 2023Article
- Exploring a Possible Interplay between Schizophrenia, Oxytocin, and Estrogens: A Narrative Review.Brain sciences · 2023Review
- Hormonal influences in migraine - interactions of oestrogen, oxytocin and CGRP.Nature reviews. Neurology · 2021Review
- Sexual Dimorphism in Glucocorticoid Stress Response.International journal of molecular sciences · 2021Review
- Androgens and Their Role in Regulating Sex Differences in the Hypothalamic/Pituitary/Adrenal Axis Stress Response and Stress-Related Behaviors.Androgens: clinical research and therapeutics · 2021Review
- Roles for androgens in mediating the sex differences of neuroendocrine and behavioral stress responses.Biology of sex differences · 2020Review
- The Hypothalamic-Pituitary-Adrenal Axis: Development, Programming Actions of Hormones, and Maternal-Fetal Interactions.Frontiers in behavioral neuroscience · 2020Review
- Neurochemical Characterization of Neurons Expressing Estrogen Receptor β in the Hypothalamic Nuclei of Rats Using in Situ Hybridization and Immunofluorescence.International journal of molecular sciences · 2019Article
- Sexual dimorphism of oxytocin and vasopressin in social cognition and behavior.Psychology research and behavior management · 2019Review
- Sex differences in the hypothalamic-pituitary-adrenal axis' response to stress: an important role for gonadal hormones.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Review
- Role of HPA and the HPG Axis Interaction in Testosterone-Mediated Learned Helpless Behavior.Molecular neurobiology · 2019Article
- The impact of oxytocin on stress: the role of sex.Current opinion in behavioral sciences · 2018Article
- Chronic Variable Stress Induces Sex-Specific Alterations in Social Behavior and Neuropeptide Expression in the Mouse.Endocrinology · 2018Article
- Distribution and chemical composition of estrogen receptor β neurons in the paraventricular nucleus of the female and male mouse hypothalamus.The Journal of comparative neurology · 2017Article
- Hypothalamic-pituitary-adrenal and hypothalamic-pituitary-gonadal axes: sex differences in regulation of stress responsivity.Stress (Amsterdam, Netherlands) · 2017Review
- Direct Involvement of Androgen Receptor in Oxytocin Gene Expression: Possible Relevance for Mood Disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017Article
- Hypothalamic transcriptional expression of the kisspeptin system and sex steroid receptors differs among polycystic ovary syndrome rat models with different endocrine phenotypes.Clinics (Sao Paulo, Brazil) · 2017Article
- Endocrine Disruption of Vasopressin Systems and Related Behaviors.Frontiers in endocrinology · 2017Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Testosterone has been shown to suppress the acute stress-induced activation of the hypothalamic-pituitary-adrenal axis; however, the mechanisms underlying this response remain unclear. The hypothalamic-pituitary-adrenal axis is regulated by a neuroendocrine subpopulation of medial parvocellular neurons in the paraventricular nucleus of the hypothalamus (PVN). These neurons are devoid of androgen receptors (ARs). Therefore, a possibility is that the PVN target neurons respond to a metabolite in the testosterone catabolic pathway via an AR-independent mechanism. The dihydrotestosterone metabolite, 5α-androstane-3β,17β-diol (3β-diol), binds and activates estrogen receptor-β (ER-β), the predominant ER in the PVN. In the PVN, ER-β is coexpressed with oxytocin (OT). Therefore, we tested the hypothesis that 3β-diol regulates OT expression through ER-β activation. Treatment of ovariectomized rats with estradiol benzoate or 3β-diol for 4 days increased OT mRNA selectively in the midcaudal, but not rostral PVN compared with vehicle-treated controls. 3β-Diol treatment also increased OT mRNA in the hypothalamic N38 cell line in vitro. The functional interactions between 3β-diol and ER-β with the human OT promoter were examined using an OT promoter-luciferase reporter construct (OT-luc). In a dose-dependent manner, 3β-diol treatment increased OT-luc activity when cells were cotransfected with ER-β, but not ER-α. The 3β-diol-induced OT-luc activity was reduced by deletion of the promoter region containing the composite hormone response element (cHRE). Point mutations of the cHRE also prevented OT-luc activation by 3β-diol. These results indicate that 3β-diol induces OT promoter activity via ER-β-cHRE interactions.
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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.