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Abstract：
It was a widely held belief that sex steroids, namely testosterone and 17β-estradiol (E2) of gonadal origin, control synaptic plasticity in the hippocampus. A new paradigm emerged when it was shown that these sex steroids are synthesized in the hippocampus. The inhibition of sex steroids in the hippocampus impairs synaptic plasticity sex-dependently in this region of the brain. In gonadectomized animals and in hippocampal cultures, inhibition of estradiol synthesis in female animals and in cultures from female animals, and inhibition of dihydrotestosterone synthesis in male animals and in cultures of male animals, cause synapse loss and impair LTP in the hippocampus, but not vice versa. Since the hippocampal cultures originated from perinatal animals, and due to the similarity of in vivo and in vitro findings, it appears that hippocampal neurons are differentiated in a sex-specific manner during the perinatal period when sexual imprinting takes place.
摘要：
人们普遍认为性类固醇，即睾丸激素和性腺来源的17β-雌二醇（E2），控制海马的突触可塑性。当发现这些性类固醇是在海马体中合成的时，出现了一种新的范例。海马中性类固醇的抑制作用会损害大脑该区域的突触可塑性。在性腺切除的动物和海马培养物中，在雌性动物和雌性动物的培养物中抑制雌二醇的合成，在雄性动物和雄性动物的培养物中抑制二氢睾酮的合成，导致突触丢失并损害海马中的LTP，但反之亦然。由于海马培养物起源于围产期动物，由于体内和体外研究结果的相似性，在围产期发生性印记时，海马神经元似乎以性别特异性方式分化。
