Genetic and Epigenetic Creation of Maleness and Femaleness

We have a better understanding of the systems that control sexual urges in the brains of animals than of humans, but there are now abundant reasons to believe the principles, if not the details, will translate well across many mammalian species (Panksepp, 1998; Pfaus, 1996). However, since the variety of sexual strategies among species is so vast (Judson, 2002), the underlying brain details will also vary. Likewise, many complexities arise from the fact that sexual motivation and performance are distinguishable, albeit highly interactive, systems in the brain (Everitt, 1990). Although there has been resistance to the use of animal work to illuminate the human condition, here we will summarize the general principles, while not denying the abundant differences in details across species (Robbins, 1996).

To a remarkable degree, male and female sexuality are subservient to many distinct as well as several overlapping brain controls (summarized in Panksepp, 1998; Pfaff,

1999). The role of the testis-determining gene on the Y chromosome in elaborating male genital development and the resulting testosterone (T) based signaling of maleness to the brain has been worked out in considerable detail, at least in rats (Pfaff, 1999). If, during the critical organizational phase of gender determination, during the last few days before birth (in humans that happens in the second trimester of gestation, and a few days before birth in rats), the cascade of biochemical events goes according to the standard schedule, the brains of males become masculinized. To be effective in precipitating this developmental cascade, the pulsatile secretions of T in utero have to be converted to the metabolite estrogen via aromatization. If sufficient estrogen (E) does not bathe the male brain at the right time (e.g., because of a mistiming of T secretion, inadequate aromatase, or deficits of estrogen receptors in the right regions of the brain), the male brain remains organized in the primordial female-typical pattern. Parenthetically, since the mother's estrogen could promote masculinization of the female brain, female fetuses have "failsafe" prophylactic molecules, such as «-fetoprotein, that can sequester maternal estrogens.

Since male-typical body organization is elaborated more by a different metabolite of T, namely dihydrotestosterone (DHT), produced via the enzyme 5-«-reductase, one can a have male-typical brain in a female-typical body, and vice versa, depending on which hormones the fetus was exposed to during the critical organizational periods of sexual differentiation. Without denying the importance of psychosocial learning on many aspects of human development, the metabolic conversion of T into E and DHT may provide some insight into trans-sexual and homosexual tendencies. Although these issues cannot be analyzed readily in the human species, there is now substantial evidence, especially from work on rodents, that male bodies can contain female-typical brains, and female bodies can contain male-typical brains in rats. There is also suggestive evidence this can occur in humans (e.g., Imperato-McGinley, et al. 1979). These realignments of brain and body gender identities, no doubt produce substantial psychological consequences during adolescence as individuals reach sexual maturity (Kimura, 1999; LeVay, et al. 1993).

What does it mean to have a masculinized brain? In animals we know this is reflected in the fact that certain neuronal groups in the anterior hypothalamus [the sexually dimorphic nuclei of the preoptic area (SDN-POA)] grow larger than in most females. Partly this is due to the slowing of early neuronal "weeding" and partly to the neural growth-promoting effects of E. There is increasing data to show that the same type of effects are present in the human brain (LeVay, et al. 1993), especially in the intermediate nuclei of the anterior hypothalamus (INAH), but other brain areas as well (Zhou et al., 1995). These morphological differences participate in the elaboration of sex-typical psychological and behavioral differences. The failure to recognize that such neurobiological organizational processes do occur in humans has been a source of prolonged distress to those who have been treated according to culturally politicized psychosocial models of gender determination (Colapinto, 2000).

One of the remarkable aspects of these psychobiological findings, at least in rats, is that environmental events, such as maternal stress, can influence the brain organizational effects of early hormone secretions. The male fetuses of mother rats that have been stressed consistently exhibit a reduction in both neural and behavioral mas-culinization. This is partly due to the fact that the fetal secretions of T are too early, before adequate aromatization enzymes are present to convert T to E, and also before the receptive elements for estrogen have matured. Conversely, female offspring tend to exhibit some masculinization as a result of maternal stress, but the mechanisms for this phenomenon have not been worked out. There is a modest amount of evidence that similar effects can occur in our own species (Ellis and Ebertz, 1997).

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