近日，来自美国和日本研究人员的一项研究结果“Membrane-Initiated Estradiol Signaling Induces Spinogenesis Required for Female Sexual Receptivity。”该项研究结果发表在国际著名杂志The Journal of Neuroscience上，研究人员通过对脑细胞间的微小神经嵴组织的研究揭示，“处男”老鼠相比那些有过性经验的老鼠有更多这种神经棘组织。
这意味着这种组织促使老鼠发生了初次性行为，并在初夜过后变少或消失。《新科学家》报告称，将来有一天可能会发明出一种能令这种神经嵴组织增加的药丸，为人类服务。这种药丸将有助于提升性欲。
美国神经学家斯图亚特-托比特说，这些研究让人们能够“一睹大脑神经嵴状结构的改变对于老鼠性能力的影响，这种影响也许可以推及包括人类在内的其他哺乳动物。”
一旦这种神经嵴组织的使命完成了，它们就不再被需要，因而也就减少或消失了。而且，据《新科学家》本周的报道，这种微小的嵴状组织还会影响男人的早期性行为。
现在已经获知人类和其他动物的几个和性行为相关的大脑区域在两性之间存在着大小之差。
为了查明性行为是否会改变男性较大的这块大脑区域，埼玉大学的研究人员将从未有过性生活的雄性老鼠和有过性经验的雄性老鼠的大脑做了比较。
他们发现，“非处”老鼠的这种大脑神经嵴组织的数量明显比“处男”老鼠要低。
研究人员冢原慎司说，神经嵴状组织的减少可能是由多种因素引起的，包括雌性出现引发的荷尔蒙的改变。他说，嵴组织也许是“学习如何性交的单行道”，一旦被使用过，它们就不再被需要。（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.
