近日,,來(lái)自美國(guó)和日本研究人員的一項(xiàng)研究結(jié)果“Membrane-Initiated Estradiol Signaling Induces Spinogenesis Required for Female Sexual Receptivity。”該項(xiàng)研究結(jié)果發(fā)表在國(guó)際著名雜志The Journal of Neuroscience上,,研究人員通過(guò)對(duì)腦細(xì)胞間的微小神經(jīng)嵴組織的研究揭示,,“處男”老鼠相比那些有過(guò)性經(jīng)驗(yàn)的老鼠有更多這種神經(jīng)棘組織。
這意味著這種組織促使老鼠發(fā)生了初次性行為,,并在初夜過(guò)后變少或消失,。《新科學(xué)家》報(bào)告稱,,將來(lái)有一天可能會(huì)發(fā)明出一種能令這種神經(jīng)嵴組織增加的藥丸,,為人類服務(wù)。這種藥丸將有助于提升性欲,。
美國(guó)神經(jīng)學(xué)家斯圖亞特-托比特說(shuō),,這些研究讓人們能夠“一睹大腦神經(jīng)嵴狀結(jié)構(gòu)的改變對(duì)于老鼠性能力的影響,這種影響也許可以推及包括人類在內(nèi)的其他哺乳動(dòng)物,。”
一旦這種神經(jīng)嵴組織的使命完成了,,它們就不再被需要,因而也就減少或消失了,。而且,,據(jù)《新科學(xué)家》本周的報(bào)道,這種微小的嵴狀組織還會(huì)影響男人的早期性行為,。
現(xiàn)在已經(jīng)獲知人類和其他動(dòng)物的幾個(gè)和性行為相關(guān)的大腦區(qū)域在兩性之間存在著大小之差,。
為了查明性行為是否會(huì)改變男性較大的這塊大腦區(qū)域,埼玉大學(xué)的研究人員將從未有過(guò)性生活的雄性老鼠和有過(guò)性經(jīng)驗(yàn)的雄性老鼠的大腦做了比較,。
他們發(fā)現(xiàn),,“非處”老鼠的這種大腦神經(jīng)嵴組織的數(shù)量明顯比“處男”老鼠要低,。
研究人員冢原慎司說(shuō),神經(jīng)嵴狀組織的減少可能是由多種因素引起的,,包括雌性出現(xiàn)引發(fā)的荷爾蒙的改變,。他說(shuō),嵴組織也許是“學(xué)習(xí)如何性交的單行道”,,一旦被使用過(guò),,它們就不再被需要。(生物谷Bioon.com)
doi:10.1523/JNEUROSCI.3030-11.2011
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Membrane-Initiated Estradiol Signaling Induces Spinogenesis Required for Female Sexual Receptivity
Amy Christensen, Phoebe Dewing, and Paul Micevych
AEstrogens have profound actions on the structure of the nervous system during development and in adulthood. One of the signature actions of estradiol is to alter the morphology of neural processes. In the hippocampus, estradiol modulates spines and cellular excitability that affect cognitive behaviors. 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 β-actin immunostaining and Golgi staining to visualize estradiol-induced changes in spine density in Long–Evans rats. Golgi impregnation was used to visualize spine shape, and then β-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 β-actin immunofluorescence and filopodial spines were increased (from 70.57 ± 1.09% to 78.01 ± 1.05%, p < 0.05). Disruption of estradiol-induced β-actin polymerization with cytochalasin D attenuated lordosis behavior, indicating the importance of estradiol-mediated spinogenesis for female sexual receptivity (81.43 ± 7.05 to 35.00 ± 11.76, p < 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.