{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T07:24:48Z","timestamp":1790753088170,"version":"4.1.0"},"reference-count":62,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2023,6,6]],"date-time":"2023-06-06T00:00:00Z","timestamp":1686009600000},"content-version":"vor","delay-in-days":5,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001505","name":"Health Research Council of New Zealand","doi-asserted-by":"publisher","award":["18\u2010671"],"award-info":[{"award-number":["18\u2010671"]}],"id":[{"id":"10.13039\/501100001505","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Neuroendocrinology"],"published-print":{"date-parts":[[2023,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Polycystic ovary syndrome (PCOS) is a female endocrine disorder that is associated with prenatal exposure to excess androgens. In prenatally androgenized (PNA) mice that model PCOS, GABAergic neural transmission to and innervation of GnRH neurons is increased. Evidence suggests that elevated GABAergic innervation originates in the arcuate nucleus (ARC). We hypothesized that GABA\u2010GnRH circuit abnormalities are a direct consequence of PNA, resulting from DHT binding to androgen receptor (AR) in the prenatal brain. However, whether prenatal ARC neurons express AR at the time of PNA treatment is presently unknown. We used RNAScope in situ hybridization to localize AR mRNA (\n                    <jats:italic>Ar<\/jats:italic>\n                    )\u2010expressing cells in healthy gestational day (GD) 17.5 female mouse brains and to assess coexpression levels in specific neuronal phenotypes. Our study revealed that less than 10% of ARC GABA cells expressed\n                    <jats:italic>Ar<\/jats:italic>\n                    . In contrast, we found that ARC kisspeptin neurons, critical regulators of GnRH neurons, were highly colocalized with\n                    <jats:italic>Ar<\/jats:italic>\n                    . Approximately 75% of ARC\n                    <jats:italic>Kiss1<\/jats:italic>\n                    \u2010expressing cells also expressed\n                    <jats:italic>Ar<\/jats:italic>\n                    at GD17.5, suggesting that ARC kisspeptin neurons are potential targets of PNA. Investigating other neuronal populations in the ARC we found that ~50% of pro\u2010opiomelanocortin (\n                    <jats:italic>Pomc<\/jats:italic>\n                    ) cells, 22% of tyrosine hydroxylase (\n                    <jats:italic>Th<\/jats:italic>\n                    ) cells, 8% of agouti\u2010related protein (\n                    <jats:italic>Agrp<\/jats:italic>\n                    ) cells and 8% of somatostatin (\n                    <jats:italic>Sst<\/jats:italic>\n                    ) cells express\n                    <jats:italic>Ar<\/jats:italic>\n                    . Lastly, RNAscope in coronal sections showed\n                    <jats:italic>Ar<\/jats:italic>\n                    expression in the medial preoptic area (mPOA), and the ventral part of the lateral septum (vLS). These\n                    <jats:italic>Ar<\/jats:italic>\n                    \u2010expressing regions were highly GABAergic, and 22% of GABA cells in the mPOA and 25% of GABA cells in the vLS also expressed\n                    <jats:italic>Ar<\/jats:italic>\n                    . Our findings identify specific neuronal phenotypes in the ARC, mPOA, and vLS that are androgen sensitive in late gestation. PNA\u2010induced functional changes in these neurons may be related to the development of impaired central mechanisms associated with PCOS\u2010like features.\n                  <\/jats:p>","DOI":"10.1111\/jne.13302","type":"journal-article","created":{"date-parts":[[2023,5,18]],"date-time":"2023-05-18T22:46:05Z","timestamp":1684449965000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Defining potential targets of prenatal androgen excess: Expression analysis of androgen receptor on hypothalamic neurons in the fetal female mouse brain"],"prefix":"10.1111","volume":"35","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6920-5360","authenticated-orcid":false,"given":"Yugo","family":"Watanabe","sequence":"first","affiliation":[{"name":"Centre for Neuroendocrinology, Department of Anatomy University of Otago School of Biomedical Sciences Dunedin New 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