ArticleEndocrinology2015
Prenatal Testosterone Treatment Leads to Changes in the Morphology of KNDy Neurons, Their Inputs, and Projections to GnRH Cells in Female Sheep.
Article in Endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Metabolic dysfunction in polycystic ovary syndrome: Pathogenic role of androgen excess and potential therapeutic strategies.Molecular metabolism · 2020Pooled it
- Kisspeptin as a test of hypothalamic dysfunction in pubertal and reproductive disorders.Andrology · 2026Review
- Regulation of ovarian function in domestic animals: translational insights into human ovarian dynamics and dysfunction.Frontiers in endocrinology · 2026Review
- Exploring the Role of Kisspeptin in Polycystic Ovary Syndrome and Its Associated Pregnancy Complications.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026Review
- Farm animal models for the study of the reproductive features of polyendocrine metabolic ovarian syndrome.Frontiers in endocrinology · 2026Review
- Neuroendocrine mechanisms responsible for elevated gonadotrophin-releasing hormone and luteinising hormone pulses in polycystic ovary syndrome.Journal of neuroendocrinology · 2025Review
- The kisspeptin system in and beyond reproduction: exploring intricate pathways and potential links between endometriosis and polycystic ovary syndrome.Reviews in endocrine & metabolic disorders · 2024Review
- Placental mRNA Expression of Neurokinin B Is Increased in PCOS Pregnancies with Female Offspring.Biomedicines · 2024Article
- Prenatal kisspeptin antagonist exposure prevents polycystic ovary syndrome development in prenatally-androgenized rats in adulthood: An experimental study.International journal of reproductive biomedicine · 2023Article
- Deletion of Androgen Receptor in LepRb Cells Improves Estrous Cycles in Prenatally Androgenized Mice.Endocrinology · 2023Article
- Prenatal Origins of Endometriosis Pathology and Pain: Reviewing the Evidence of a Role for Low Testosterone.Journal of pain research · 2023Article
- Impaired steroid hormone feedback in polycystic ovary syndrome: Evidence from preclinical models for abnormalities within central circuits controlling fertility.Clinical endocrinology · 2022Review
- Early programming of reproductive health and fertility: novel neuroendocrine mechanisms and implications in reproductive medicine.Human reproduction update · 2022Review
- Highlights of neuroanatomical discoveries of the mammalian gonadotropin-releasing hormone system.Journal of neuroendocrinology · 2022Review
- The role of gonadotropin-releasing hormone neurons in polycystic ovary syndrome.Journal of neuroendocrinology · 2022Review
- Prenatal androgen treatment impairs the suprachiasmatic nucleus arginine-vasopressin to kisspeptin neuron circuit in female mice.Frontiers in endocrinology · 2022Article
- Evidence that synaptic plasticity of glutamatergic inputs onto KNDy neurones during the ovine follicular phase is dependent on increasing levels of oestradiol.Journal of neuroendocrinology · 2021Article
- Clinical Applications of Serum Anti-Müllerian Hormone Measurements in Both Males and Females: An Update.Innovation (Cambridge (Mass.)) · 2021Review
- Developmental programming: gestational testosterone excess disrupts LH secretion in the female sheep fetus.Reproductive biology and endocrinology : RB&E · 2020Article
- Animal Models to Understand the Etiology and Pathophysiology of Polycystic Ovary Syndrome.Endocrine reviews · 2020Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Prenatal testosterone (T)-treated ewes display a constellation of reproductive defects that closely mirror those seen in PCOS women, including altered hormonal feedback control of GnRH. Kisspeptin/neurokinin B/dynorphin (KNDy) neurons of the arcuate nucleus (ARC) play a key role in steroid feedback control of GnRH secretion, and prenatal T treatment in sheep causes an imbalance of KNDy peptide expression within the ARC. In the present study, we tested the hypothesis that prenatal T exposure, in addition to altering KNDy peptides, leads to changes in the morphology and synaptic inputs of this population, kisspeptin cells of the preoptic area (POA), and GnRH cells. Prenatal T treatment significantly increased the size of KNDy cell somas, whereas POA kisspeptin, GnRH, agouti-related peptide, and proopiomelanocortin neurons were each unchanged in size. Prenatal T treatment also significantly reduced the total number of synaptic inputs onto KNDy neurons and POA kisspeptin neurons; for KNDy neurons, the decrease was partly due to a decrease in KNDy-KNDy synapses, whereas KNDy inputs to POA kisspeptin cells were unaltered. Finally, prenatal T reduced the total number of inputs to GnRH cells in both the POA and medial basal hypothalamus, and this change was in part due to a decreased number of inputs from KNDy neurons. The hypertrophy of KNDy cells in prenatal T sheep resembles that seen in ARC kisspeptin cells of postmenopausal women, and together with changes in their synaptic inputs and projections to GnRH neurons, may contribute to defects in steroidal control of GnRH observed in this animal model.
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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.