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While ovariectomy (OVX) induced a comparable luteinizing hormone (LH) increase in both wild\u2010type and C451A\u2010ER\u03b1 females, C451A\u2010ER\u03b1 females failed to respond to chronic estradiol (E\n                    <jats:sub>2<\/jats:sub>\n                    ) (1\u2009\u03bcg) exposure, indicating dysregulated negative feedback. This lack of LH regulation in C451A\u2010ER\u03b1 females was mirrored by an absence of change in the number of neurons immunoreactive (ir) for kisspeptin (Kp) in both the rostral periventricular area of the third ventricle (RP3V) and the arcuate nucleus (ARC), for progesterone receptor (PR)\u2010ir nuclei in the preoptic area and hypothalamus, and for neurokinin 3 receptor (NK\n                    <jats:sub>3<\/jats:sub>\n                    R) in the ARC. Interestingly, increasing the dose of E\n                    <jats:sub>2<\/jats:sub>\n                    to 5\u2009\u03bcg restored normal negative feedback and normal numbers of Kp\u2010ir neurons and PR\u2010ir nuclei, but not the surface covered by Kp\u2010ir fibers and the number of NK\n                    <jats:sub>3<\/jats:sub>\n                    R\u2010ir neurons in the ARC. By contrast, E\n                    <jats:sub>4<\/jats:sub>\n                    mimicked the negative feedback of E\n                    <jats:sub>2<\/jats:sub>\n                    on circulating LH in OVX WT females following both acute and chronic treatment and potentiated rather than blocked the effects of E\n                    <jats:sub>2<\/jats:sub>\n                    when administered along with it. E\n                    <jats:sub>4<\/jats:sub>\n                    also mimicked the stimulatory effects of E\n                    <jats:sub>2<\/jats:sub>\n                    on the number of PR\u2010ir nuclei in several preoptic and hypothalamic regions and the percentage of area covered by Kp\u2010ir material in the ARC, as well as its inhibitory action on the number of Kp\u2010ir neurons in the ARC. Therefore, the C451A\u2010ER\u03b1 mutation interferes with the control of the negative feedback through distinct mechanisms differing by their dose\u2010dependency to E\n                    <jats:sub>2<\/jats:sub>\n                    . By contrast, E\n                    <jats:sub>4<\/jats:sub>\n                    mimicked all effects of E\n                    <jats:sub>2<\/jats:sub>\n                    on the negative feedback and the associated neural circuits, indicating that E\n                    <jats:sub>4<\/jats:sub>\n                    acts as a weak ER\u03b1 agonist in this context. Together, these results suggest that C451A\u2010ER\u03b1 modifies the sensitivity to E\n                    <jats:sub>2<\/jats:sub>\n                    , impacting the negative feedback of E\n                    <jats:sub>2<\/jats:sub>\n                    on LH regulation.\n                  <\/jats:p>","DOI":"10.1111\/jne.70016","type":"journal-article","created":{"date-parts":[[2025,3,30]],"date-time":"2025-03-30T07:42:53Z","timestamp":1743320573000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Role of membrane estrogen receptor alpha on the negative feedback of estrogens on\n                    <scp>luteinizing hormone<\/scp>\n                    secretion"],"prefix":"10.1111","volume":"37","author":[{"given":"M\u00e9lanie C.","family":"Faure","sequence":"first","affiliation":[{"name":"Laboratory of Neuroendocrinology, GIGA Neurosciences University of Li\u00e8ge  Li\u00e8ge 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