{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T23:33:36Z","timestamp":1790984016264,"version":"4.1.0"},"reference-count":74,"publisher":"The Endocrine Society","issue":"11","license":[{"start":{"date-parts":[[2020,8,31]],"date-time":"2020-08-31T00:00:00Z","timestamp":1598832000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001505","name":"Health Research Council of New Zealand","doi-asserted-by":"publisher","award":["15\u2013097"],"award-info":[{"award-number":["15\u2013097"]}],"id":[{"id":"10.13039\/501100001505","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001505","name":"Health Research Council of New Zealand","doi-asserted-by":"publisher","award":["18\u2013671"],"award-info":[{"award-number":["18\u2013671"]}],"id":[{"id":"10.13039\/501100001505","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Royal Society Marsden Fund","award":["14\u2013077"],"award-info":[{"award-number":["14\u2013077"]}]},{"name":"Royal Society Marsden Fund","award":["17\u2013064"],"award-info":[{"award-number":["17\u2013064"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Polycystic ovary syndrome (PCOS), the most common form of anovulatory infertility, is associated with altered signaling within the hormone-sensitive neuronal network that regulates gonadotropin-releasing hormone (GnRH) neurons, leading to a pathological increase in GnRH secretion. Circuit remodeling is evident between GABAergic neurons in the arcuate nucleus (ARN) and GnRH neurons in a murine model of PCOS. One-third of ARN GABA neurons co-express neuropeptide Y (NPY), which has a known yet complex role in regulating GnRH neurons and reproductive function. Here, we investigated whether the NPY-expressing subpopulation (NPYARN) of ARN GABA neurons (GABAARN) is also affected in prenatally androgenized (PNA) PCOS-like NPYARN reporter mice [Agouti-related protein (AgRP)-Cre;\u03c4GFP]. PCOS-like mice and controls were generated by exposure to di-hydrotestosterone or vehicle (VEH) in late gestation. \u03c4GFP-expressing NPYARN neuron fiber appositions with GnRH neurons and gonadal steroid hormone receptor expression in \u03c4GFP-expressing NPYARN neurons were assessed using confocal microscopy. Although GnRH neurons received abundant close contacts from \u03c4GFP-expressing NPYARN neuron fibers, the number and density of putative inputs was not affected by prenatal androgen excess. NPYARN neurons did not co-express progesterone receptor or estrogen receptor \u03b1 in either PNA or VEH mice. However, the proportion of NPYARN neurons co-expressing the androgen receptor was significantly elevated in PNA mice. Therefore, NPYARN neurons are not remodeled by prenatal androgen excess like the wider GABAARN population, indicating GABA-to-GnRH neuron circuit remodeling occurs in a presently unidentified non-NPY\/AgRP population of GABAARN neurons. NPYARN neurons do, however, show independent changes in the form of elevated androgen sensitivity.<\/jats:p>","DOI":"10.1210\/jendso\/bvaa129","type":"journal-article","created":{"date-parts":[[2020,8,31]],"date-time":"2020-08-31T18:02:09Z","timestamp":1598896929000},"source":"Crossref","is-referenced-by-count":25,"title":["Investigating the NPY\/AgRP\/GABA to GnRH Neuron Circuit in Prenatally Androgenized PCOS-Like Mice"],"prefix":"10.1210","volume":"4","author":[{"given":"Christopher J","family":"Marshall","sequence":"first","affiliation":[{"name":"Centre for Neuroendocrinology and Department of Physiology, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melanie","family":"Prescott","sequence":"additional","affiliation":[{"name":"Centre for Neuroendocrinology and Department of Physiology, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand"}],"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 for Neuroendocrinology and Department of Physiology, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"80","published-online":{"date-parts":[[2020,8,31]]},"reference":[{"issue":"1","key":"2020111902563206100_CIT0001","doi-asserted-by":"crossref","first-page":"6","DOI":"10.1016\/j.fertnstert.2016.05.003","article-title":"Criteria, prevalence, and phenotypes of polycystic ovary syndrome","volume":"106","author":"Lizneva","year":"2016","journal-title":"Fertil Steril."},{"issue":"8","key":"2020111902563206100_CIT0002","doi-asserted-by":"crossref","first-page":"2107","DOI":"10.1093\/oxfordjournals.humrep.a136243","article-title":"Polycystic ovary syndrome: the spectrum 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