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In the hypothalamus, estradiol increases spine density in mediobasal hypothalamic nuclei that regulate reproduction. The hypothalamic arcuate nucleus (ARH), an important site for modulation of female sexual receptivity, has a sexual dimorphism in dendritic spine density that favors females. In the present study, we used both \u03b2-actin immunostaining and Golgi staining to visualize estradiol-induced changes in spine density in Long\u2013Evans rats. Golgi impregnation was used to visualize spine shape, and then \u03b2-actin immunoreactivity was used as a semiquantitative measure of spine plasticity since actin forms the core of dendritic spines. At 4 h after estradiol treatment, both \u03b2-actin immunofluorescence and filopodial spines were increased (from 70.57 \u00b1 1.09% to 78.01 \u00b1 1.05%,<jats:italic>p<\/jats:italic>&lt; 0.05). Disruption of estradiol-induced \u03b2-actin polymerization with cytochalasin D attenuated lordosis behavior, indicating the importance of estradiol-mediated spinogenesis for female sexual receptivity (81.43 \u00b1 7.05 to 35.00 \u00b1 11.76,<jats:italic>p<\/jats:italic>&lt; 0.05). Deactivation of cofilin, an actin depolymerizing factor is required for spinogenesis. Membrane-initiated estradiol signaling involving the metabotropic glutamate receptor 1a was responsible for the phosphorylation and thereby deactivation of cofilin. These data demonstrate that estradiol-induced spinogenesis in the ARH is an important cellular mechanism for the regulation of female sexual behavior.<\/jats:p>","DOI":"10.1523\/jneurosci.3030-11.2011","type":"journal-article","created":{"date-parts":[[2011,12,2]],"date-time":"2011-12-02T10:13:58Z","timestamp":1322820838000},"page":"17583-17589","source":"Crossref","is-referenced-by-count":83,"title":["Membrane-Initiated Estradiol Signaling Induces Spinogenesis Required for Female Sexual 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