{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T12:18:30Z","timestamp":1790770710434,"version":"4.1.0"},"reference-count":65,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2022,12,1]],"date-time":"2022-12-01T00:00:00Z","timestamp":1669852800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Neuroendocrinology"],"published-print":{"date-parts":[[2022,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Prader\u2013Willi syndrome (PWS) is a neurodevelopmental disorder characterized by hyperphagia, obesity, developmental delay and intellectual disability. Studies suggest dysfunctional signaling of the neuropeptide oxytocin as one of the key mechanisms in PWS, and administration of oxytocin via intranasal or systemic routes yielded promising results in both humans and mouse models. However, a detailed assessment of the oxytocin system in mouse models of PWS such as the Magel2\u2010deficient\n                    <jats:italic>Magel2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>tm1.Stw<\/jats:italic>\n                    <\/jats:sup>\n                    mouse, is lacking. In the present study, we performed an automated counting of oxytocin cells in the entire paraventricular nucleus of the hypothalamus of\n                    <jats:italic>Magel2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>tm1.Stw<\/jats:italic>\n                    <\/jats:sup>\n                    and wild\u2010type control mice and found a significant reduction in the caudal part, which represents the parvocellular subdivision. In addition, based on the recent discovery that some astrocytes express the oxytocin receptor (OTR), we performed detailed analysis of astrocyte numbers and morphology in various brain regions, and assessed expression levels of the astrocyte marker glial fibrillary acidic protein, which was significantly decreased in the hypothalamus, but not other brain regions in\n                    <jats:italic>Magel2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>tm1.Stw<\/jats:italic>\n                    <\/jats:sup>\n                    mice. Finally, we analyzed the number of OTR\u2010expressing astrocytes in various brain regions and found a significant reduction in the nucleus accumbens of\n                    <jats:italic>Magel2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>tm1.Stw<\/jats:italic>\n                    <\/jats:sup>\n                    mice, as well as a sex\u2010specific difference in the lateral septum. This study suggests a role for caudal paraventricular nucleus oxytocin neurons as well as OTR\u2010expressing astrocytes in a mouse model of PWS, provides novel information about sex\u2010specific expression of astrocytic OTRs, and presents several new brain regions containing OTR\u2010expressing astrocytes in the mouse brain.\n                  <\/jats:p>","DOI":"10.1111\/jne.13217","type":"journal-article","created":{"date-parts":[[2022,11,15]],"date-time":"2022-11-15T01:01:33Z","timestamp":1668474093000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["Analysis of the hypothalamic oxytocin system and oxytocin receptor\u2010expressing astrocytes in a mouse model of\n                    <scp>Prader\u2013Willi<\/scp>\n                    syndrome"],"prefix":"10.1111","volume":"34","author":[{"given":"Ferdinand","family":"Althammer","sequence":"first","affiliation":[{"name":"Institute of Human Genetics Heidelberg 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Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tim","family":"Schubert","sequence":"additional","affiliation":[{"name":"Institute of Human Genetics Heidelberg University  Heidelberg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6960-7685","authenticated-orcid":false,"given":"Matthew K.","family":"Kirchner","sequence":"additional","affiliation":[{"name":"Center for Neuroinflammation and Cardiometabolic Diseases Georgia State University  Atlanta GA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Javier E.","family":"Stern","sequence":"additional","affiliation":[{"name":"Center for Neuroinflammation and Cardiometabolic Diseases Georgia State University  Atlanta GA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexandre","family":"Charlet","sequence":"additional","affiliation":[{"name":"Centre National de la Recherche Scientifique and University of Strasbourg, 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