influences of male partners on women’s sexual activity. However, there is evidence for changes in the level of female sexual desire in women with a peak at midcycle (Bancroft et al., 1983; Dennerstein et al., 1994; Stanislaw and Rice, 1988; Van Goozen et al., 1997). Thus, although hormones are not necessary for female sexual behavior, there is accumulating evidence that hormones modulate sexual desire (Meston and Frolich, 2000; Wallen, 2001). Further studies are needed to understand the differential roles of estrogens and androgens in this regard. As discussed for the male, there is also evidence that social factors interact with hormonal influences with regard to sexual behavior in females. Adams et al. (1997) showed that women who used less reliable contraceptives showed less pronounced midcycle increases in heterosexual initiation, but much greater midcycle increases in autosexual behavior.

HORMONAL CHANGES THROUGH THE LIFE SPAN

Early-Life Activation of the Reproductive Axis

Early in embryonic development the components of the reproductive axis are formed and become functional. GnRH neurons, which provide the central drive to the reproductive axis, are an unusual neuronal population in that they originate from outside the central nervous system, coming originally from the epithelial tissue of the nasal placode (Schwanzel-Fukuda and Pfaff, 1989; Wray et al., 1989). During embryonic development, GnRH neurons migrate across the surface of the brain into the hypothalamus. Migration is dependent on a scaffolding of neurons and glial cells along which the GnRH neurons move, with chemical signals guiding the process (Silverman et al., 1994). Failure of GnRH neurons to properly migrate leads to a clinical condition, Kallman’s syndrome, in which GnRH neuroendocrine neurons do not reach their final destination and thus do not stimulate pituitary gonadotropin secretion (Schwanzel-Fukuda et al., 1989). Patients with Kallman’s syndrome do not spontaneously enter puberty. Administration of exogenous GnRH effectively treats this form of hypothalamic hypogonadism, although, as discussed above, this requires pulsatile administration of GnRH.

Functional activity of the reproductive axis as a whole is initiated during fetal development, and surprisingly by midgestation circulating levels of LH and FSH reach values similar to those found in adulthood (Ellinwood and Resko, 1984; Kaplan et al., 1976). Later in gestational development the gonadotropin levels decline, restrained by rising levels of circulating gonadal steroids (Kaplan et al., 1976; Resko and Ellinwood, 1985). The steroids having this effect are likely placental in origin, in that following parturition there is a rise in circulating gonadotropin levels that is apparent



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