Cooke B, Hegstrom C D, Villeneuve L S, Breedlove S M
Department of Psychology, University of California, Berkeley, California 94720-1650, USA.
Front Neuroendocrinol. 1998 Oct;19(4):323-62. doi: 10.1006/frne.1998.0171.
A wide variety of sexual dimorphisms, structural differences between the sexes, have been described in the brains of many vertebrate species, including humans. In animal models of neural sexual dimorphism, gonadal steroid hormones, specifically androgens, play a crucial role in engendering these differences by masculinizing the nervous system of males. Usually, the androgen must act early in life, often during the fetal period to masculinize the nervous system and behavior. However, there are a few examples of androgen, in adulthood, masculinizing both the structure of the nervous system and behavior. In the modal pattern, androgens are required both during development and adulthood to fully masculinize brain structure and behavior. In rodent models of neural sexual dimorphism, it is often the aromatized metabolites of androgen, i.e., estrogens, which interact with estrogen receptors to masculinize the brain, but there is little evidence that aromatized metabolites of androgen play this role in primates, including humans. There are other animal models where androgens themselves masculinize the nervous system through interaction with androgen receptors. In the course of masculinizing the nervous system, steroids can affect a wide variety of cellular mechanisms, including neurogenesis, cell death, cell migration, synapse formation, synapse elimination, and cell differentiation. In animal models, there are no known examples where only a single neural center displays sexual dimorphism. Rather, each case of sexual dimorphism seems to be part of a distributed network of sexually dimorphic neuronal populations which normally interact with each other. Finally, there is ample evidence of sexual dimorphism in the human brain, as sex differences in behavior would require, but there has not yet been any definitive proof that steroids acting early in development directly masculinize the human brain.
在包括人类在内的许多脊椎动物的大脑中，已经描述了各种各样的性二态性，即两性之间的结构差异。在神经性别二态性的动物模型中，性腺类固醇激素，特别是雄激素，通过使雄性神经系统男性化，在产生这些差异中起着关键作用。通常，雄激素必须在生命早期起作用，通常是在胎儿期，以使神经系统和行为男性化。然而，也有一些雄激素在成年期使神经系统结构和行为都男性化的例子。在典型模式中，雄激素在发育和成年期都需要，才能使脑结构和行为完全男性化。在神经性别二态性的啮齿动物模型中，通常是雄激素的芳香化代谢产物，即雌激素，与雌激素受体相互作用，使大脑男性化，但几乎没有证据表明雄激素的芳香化代谢产物在包括人类在内的灵长类动物中起这种作用。还有其他动物模型，其中雄激素本身通过与雄激素受体相互作用使神经系统男性化。在使神经系统男性化的过程中，类固醇可以影响多种细胞机制，包括神经发生、细胞死亡、细胞迁移、突触形成、突触消除和细胞分化。在动物模型中，没有已知的例子表明只有一个神经中枢表现出性别二态性。相反，每一个性别二态性的例子似乎都是一个由性别二态性神经元群体组成的分布式网络的一部分，这些群体通常相互作用。最后，有充分的证据表明人类大脑中存在性别二态性，正如行为上的性别差异所要求的那样，但尚未有任何确凿的证据表明发育早期起作用的类固醇直接使人类大脑男性化。
