{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T23:33:33Z","timestamp":1790984013515,"version":"4.1.0"},"reference-count":59,"publisher":"The Endocrine Society","issue":"7","license":[{"start":{"date-parts":[[2024,5,24]],"date-time":"2024-05-24T00:00:00Z","timestamp":1716508800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"New Zealand Health Research Council Program","award":["18-671"],"award-info":[{"award-number":["18-671"]}]},{"name":"Royal Society Marsden Fund","award":["17-064"],"award-info":[{"award-number":["17-064"]}]},{"name":"Australian National Health and Medical Research Council","award":["APP1158540"],"award-info":[{"award-number":["APP1158540"]}]},{"name":"Centre for Research Excellence in Polycystic Ovary Syndrome"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,5,27]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Androgen excess is a hallmark feature of polycystic ovary syndrome (PCOS), the most common form of anovulatory infertility. Clinical and preclinical evidence links developmental or chronic exposure to hyperandrogenism with programming and evoking the reproductive and metabolic traits of PCOS. While critical androgen targets remain to be determined, central GABAergic neurons are postulated to be involved. Here, we tested the hypothesis that androgen signaling in GABAergic neurons is critical in PCOS pathogenesis in 2 well-characterized hyperandrogenic mouse models of PCOS. Using cre-lox transgenics, GABA-specific androgen receptor knockout (GABARKO) mice were generated and exposed to either acute prenatal androgen excess (PNA) or chronic peripubertal androgen excess (PPA). Females were phenotyped for reproductive and metabolic features associated with each model and brains of PNA mice were assessed for elevated GABAergic input to gonadotropin-releasing hormone (GnRH) neurons. Reproductive and metabolic dysfunction induced by PPA, including acyclicity, absence of corpora lutea, obesity, adipocyte hypertrophy, and impaired glucose homeostasis, was not different between GABARKO and wild-type (WT) mice. In PNA mice, acyclicity remained in GABARKO mice while ovarian morphology and luteinizing hormone secretion was not significantly impacted by PNA or genotype. However, PNA predictably increased the density of putative GABAergic synapses to GnRH neurons in adult WT mice, and this PNA-induced plasticity was absent in GABARKO mice. Together, these findings suggest that while direct androgen signaling in GABA neurons is largely not required for the development of PCOS-like traits in androgenized models of PCOS, developmental programming of GnRH neuron innervation is dependent upon androgen signaling in GABA neurons.<\/jats:p>","DOI":"10.1210\/endocr\/bqae060","type":"journal-article","created":{"date-parts":[[2024,5,24]],"date-time":"2024-05-24T20:37:54Z","timestamp":1716583074000},"source":"Crossref","is-referenced-by-count":20,"title":["Investigating GABA Neuron\u2013Specific Androgen Receptor Knockout in two Hyperandrogenic Models of PCOS"],"prefix":"10.1210","volume":"165","author":[{"given":"Irene E","family":"Sucquart","sequence":"first","affiliation":[{"name":"Fertility & Research Centre, School of Clinical Medicine, University of New South Wales Sydney , Randwick, NSW 2031 , Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chris","family":"Coyle","sequence":"additional","affiliation":[{"name":"Centre of Neuroendocrinology and Department of Physiology, School of Biomedical Sciences, University of Otago , Dunedin , New Zealand 9054"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0880-6661","authenticated-orcid":false,"given":"Valentina","family":"Rodriguez Paris","sequence":"additional","affiliation":[{"name":"Fertility & Research Centre, School of Clinical Medicine, University of New South Wales Sydney , Randwick, NSW 2031 , Australia"},{"name":"School of Biomedical Sciences, University of New South Wales Sydney , Randwick, NSW 2052 , Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melanie","family":"Prescott","sequence":"additional","affiliation":[{"name":"Centre of Neuroendocrinology and Department of Physiology, School of Biomedical Sciences, University of Otago , Dunedin , New Zealand 9054"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kelly A","family":"Glendining","sequence":"additional","affiliation":[{"name":"Centre of Neuroendocrinology and Department of Physiology, School of Biomedical Sciences, University of Otago , Dunedin , New Zealand 9054"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kyoko","family":"Potapov","sequence":"additional","affiliation":[{"name":"Centre of Neuroendocrinology and Department of Physiology, School of Biomedical Sciences, University of Otago , Dunedin , New Zealand 9054"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4551-2697","authenticated-orcid":false,"given":"Denovan P","family":"Begg","sequence":"additional","affiliation":[{"name":"Department of Behavioural Neuroscience, School of Psychology, University of New South Wales Sydney , Randwick, NSW , Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert B","family":"Gilchrist","sequence":"additional","affiliation":[{"name":"Fertility & Research Centre, School of Clinical Medicine, University of New South Wales Sydney , Randwick, NSW 2031 , Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kirsty A","family":"Walters","sequence":"additional","affiliation":[{"name":"Fertility & Research Centre, School of Clinical Medicine, University of New South Wales Sydney , Randwick, NSW 2031 , Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0309-532X","authenticated-orcid":false,"given":"Rebecca E","family":"Campbell","sequence":"additional","affiliation":[{"name":"Centre of Neuroendocrinology and Department of Physiology, School of Biomedical Sciences, University of Otago , Dunedin , New Zealand 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