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Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Neuroscience. 2nd edition. Sunderland (MA): Sinauer Associates; 2001.

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Neuroscience. 2nd edition.

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Hormonal Influences on Sexual Dimorphism

The development of sexual dimorphisms in the central nervous system is ultimately an outcome of genotypic sex. Genotype normally determines the phenotype of the gonads; and the gonads, in turn, are responsible for producing most of the circulating sex hormones (see Box A). Because the gonads are dimorphic, the production of sex steroids during development is itself dimorphic: The testes synthesize androgens and the ovaries estrogens. The resulting differences in circulating hormones lead to a variety of differential effects on the development of XX and XY individuals (as well as other genotypes), including physical appearance, response to pharmacological treatments, susceptibility to certain diseases, and the development of the brain.

In general, the establishment of phenotypic dimorphisms in rodents (and presumably humans) is generated by different levels of hormones at specific times in XX and XY individuals. Males have an early surge of testosterone, and females a later surge of estrogens. Paradoxically, the testosterone surge in males has the same effect as an estrogen surge, because neurons contain an enzyme (aromatase) that converts testosterone to estradiol, a form of estrogen (Figure 30.1). Thus, the surge of testosterone in developing males is, ultimately, converted into a surge of estradiol. Although testosterone is popularly considered the “male” hormone and estrogen the “female” hormone, the active agent in the brains of both males and females is estradiol. Once the conversion of testosterone has occurred, estradiol can influence gene transcription by binding with intracellular receptors (the α- and β-estrogen receptors) that in turn bind to hormone-responsive regions of DNA (Box C).

Figure 30.1. All sex steroids are synthesized from cholesterol.

Figure 30.1

All sex steroids are synthesized from cholesterol. Cholesterol is first converted to progesterone, the common precursor, by four enzymatic reactions (represented by the four arrows). Progesterone can then be converted into testosterone via another series (more...)

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Box C

The Actions of Sex Hormones. Sex hormones, which include progestagens, androgens, and estrogens, are all steroids derived from a common precursor, cholesterol (see Figure 30.1). Despite the tendency to speak of these hormones as female or male, it is (more...)

It is important during development, therefore, to sequester all exogenous sources of circulating hormones that might interfere with sexual differentiation. One such source is the maternal blood supply, which is rich in estrogens produced by the mother's gonads and placenta. To counter potential interference from this source, mammals have a circulating protein called α-fetoprotein that binds circulating estrogens. As a result, the female brain is kept from early exposure to estrogens in large amounts since they are complexed by α-fetoprotein; the male brain, however, is exposed to estrogens because the early testosterone surge is not affected by α-fetoprotein and can thus be aromatized to estradiol once inside neurons.

In sum, the way that estrogens—the ultimate agents of both female and male sexual differentiation—stimulate sexually dimorphic patterns of development is by binding to estrogen receptors. These receptors, which are transcription factors activated by estrogen binding, can then influence gene transcription and subsequently the development of an array of targets, including sexually dimorphic neural circuits.

By agreement with the publisher, this book is accessible by the search feature, but cannot be browsed.

Copyright © 2001, Sinauer Associates, Inc.
Bookshelf ID: NBK11161


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