Elaine Bonleon de Castro, 1998
Most, if not all, species with two sexes exhibit sexually dimorphic behavior and physical characteristics. These dimorphisms can be attributed to differences in the brain, such as size or function of structure, and these brain structures can be affected by the hormones circulated throughout the organism. It has been held that the sexual dimorphisms rely only on the presence or absence of androgen, namely, testosterone, during the critical period of development for an organism; however, new research suggests that the presence of estrogen has an active role in sexual differentiation.
In rats, a region known as the sexually dimorphic nucleus of the preoptic area (SDN-POA) is larger in males, and administering testosterone to a female rat can increase the size of her SDN-POA. (2) The SDN-POA was said to develop in a female fashion without hormones. More recent experiments concur that a female rat pup treated with androgen will develop a larger SDN-POA, similar in size to that of a male. However, the absence of estrogen (caused by the administration of an estrogen antagonist) caused the size of the SDN-POA to decrease. This is some evidence that estrogen does not play a passive role in the critical period. This is also an example of defeminization without masculinization.
It has also been noted that in male rat pups, testosterone is secreted by the testes, but it is converted to estrogen within neurons before causing developmental effects in males. Although female rat pups are also exposed to estrogen during this period, they are not masculinized; instead, they are protected by alpha-fetoprotein (AFP), which binds to estrogen and prevents it from entering the cells. Levels of AFP reach a maximum during the same period that testosterone and other androgens cause maximum masculinization.
When administering synthetic estrogen (diethylstilbestrol), the SDN-POA still increases in size because this hormone does not bind to AFP. The ovaries in female rat pups do not take an active role until the AFP levels have already declined. Thus, both sexes of rat pups are exposed to estrogen which causes masculine development, except females are protected by AFP. Also, estrogen biosynthesis holds a crucial role in sexual differentiation. This data contradicts the hypotheses that claim female development is a default mechanism (since an extra process is required to keep a pup from masculinization) and that testosterone is the critical factor in sexual differentiation.