{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,28]],"date-time":"2026-01-28T10:45:02Z","timestamp":1769597102906,"version":"3.49.0"},"reference-count":0,"publisher":"S. Karger AG","issue":"3","license":[{"start":{"date-parts":[[2016,4,15]],"date-time":"2016-04-15T00:00:00Z","timestamp":1460678400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2016,4,15]],"date-time":"2016-04-15T00:00:00Z","timestamp":1460678400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neuroendocrinology"],"published-print":{"date-parts":[[2017]]},"abstract":"<jats:p>Hypertension in male and aging female rodents is associated with glutamate-dependent plasticity in the hypothalamus, but existing models have failed to capture distinct transitional menopausal phases that could have a significant impact on the synaptic plasticity and emergent hypertension. In rodents, accelerated ovarian failure (AOF) induced by systemic injection of 4-vinylcyclohexane diepoxide mimics the estrogen fluctuations seen in human menopause including the perimenopause transition (peri-AOF) and postmenopause (post-AOF). Thus, we used the mouse AOF model to determine the impact of slow-pressor angiotensin II (AngII) administration on blood pressure and on the subcellular distribution of obligatory N-methyl-&lt;smlcap&gt;D&lt;\/smlcap&gt;-aspartate (NMDA) receptor GluN1 subunits in the paraventricular hypothalamic nucleus (PVN), a key estrogen-responsive cardiovascular regulatory area. Estrogen-sensitive neuronal profiles were identified in mice expressing enhanced green fluorescent protein under the promoter for estrogen receptor (ER) \u03b2, a major ER in the PVN. Slow-pressor AngII increased arterial blood pressure in mice at peri- and post-AOF time points. In control oil-injected (nonhypertensive) mice, AngII decreased the total number of GluN1 in ER\u03b2-containing PVN dendrites. In contrast, AngII resulted in a reapportionment of GluN1 from the cytoplasm to the plasma membrane of ER\u03b2-containing PVN dendrites in peri-AOF mice. Moreover, in post-AOF mice, AngII increased total GluN1, dendritic size and radical production in ER\u03b2-containing neurons. These results indicate that unique patterns of hypothalamic glutamate receptor plasticity and dendritic structure accompany the elevated blood pressure in peri- and post-AOF time points. Our findings suggest the possibility that distinct neurobiological processes are associated with the increased blood pressure during perimenopausal and postmenopausal periods.<\/jats:p>","DOI":"10.1159\/000446073","type":"journal-article","created":{"date-parts":[[2016,4,14]],"date-time":"2016-04-14T21:03:19Z","timestamp":1460667799000},"page":"239-256","source":"Crossref","is-referenced-by-count":28,"title":["Redistribution of NMDA Receptors in Estrogen-Receptor-\u03b2-Containing Paraventricular Hypothalamic Neurons following Slow-Pressor Angiotensin II Hypertension in Female Mice with Accelerated Ovarian Failure"],"prefix":"10.1159","volume":"104","author":[{"given":"Jose","family":"Marques-Lopes","sequence":"first","affiliation":[]},{"given":"Ephrath","family":"Tesfaye","sequence":"additional","affiliation":[]},{"given":"Sigal","family":"Israilov","sequence":"additional","affiliation":[]},{"given":"Tracey A.","family":"Van Kempen","sequence":"additional","affiliation":[]},{"given":"Gang","family":"Wang","sequence":"additional","affiliation":[]},{"given":"Michael J.","family":"Glass","sequence":"additional","affiliation":[]},{"given":"Virginia M.","family":"Pickel","sequence":"additional","affiliation":[]},{"given":"Costantino","family":"Iadecola","sequence":"additional","affiliation":[]},{"given":"Elizabeth M.","family":"Waters","sequence":"additional","affiliation":[]},{"given":"Teresa A.","family":"Milner","sequence":"additional","affiliation":[]}],"member":"127","published-online":{"date-parts":[[2016,4,15]]},"container-title":["Neuroendocrinology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/446073","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/446073","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,23]],"date-time":"2025-04-23T18:04:31Z","timestamp":1745431471000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000446073"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2016,4,15]]},"references-count":0,"journal-issue":{"issue":"3","published-online":{"date-parts":[[2017,3,8]]}},"URL":"https:\/\/doi.org\/10.1159\/000446073","archive":["Portico"],"relation":{"is-supplemented-by":[{"id-type":"doi","id":"10.6084\/m9.figshare.4733011","asserted-by":"subject"}]},"ISSN":["0028-3835","1423-0194"],"issn-type":[{"value":"0028-3835","type":"print"},{"value":"1423-0194","type":"electronic"}],"subject":[],"published":{"date-parts":[[2016,4,15]]}}}