Independent masculinization of neuroendocrine systems by intracerebral implants of testosterone or estradiol in the neonatal female rat

Abstract

Small pellets of testosterone (T) or estradiol (E 2), but not cholesterol (CH), when implanted into the brain of neonatal female rats on day 2 or day 5 of life, produce masculinization of the adult regulation of gonadotropic hormone (GTH) release, female sexual behavior or masculine sexual behavior, specific to the site and time of implantation and the hormone implanted. Site specificity: There appear to be specific neuronal sites where implantation of T or E 2 produces independent masculinization of GTH, female sexual behavior or masculine sexual behavior patterns. Implants of T or E 2 placed in the dorsal preoptic area (POA) perinatally increase the amount of masculine sexual behavior displayed by adults. On the other hand, the ventromedial hypothalamus (VMH) is the only area in which neonatal implants of T or E 2 produce GTH acyclicity in adults. Female sexual behavior is affected in opposite directions by hormonal implants in two different areas. Neonatal implants of T or E 2 in the POA increase adult behavioral responsiveness to estradiol benzoate (EB) alone, whereas implants in the VMH decrease adult responsiveness to EB plus progesterone therapy. Temporal speficity: The most effective time for augmenting masculine sexual behavior is before day 5, since hormone implants on that day produce marginal effects on male sexual behavior, whereas day 2 implants in the POA result in substantial increases in both mount and intromission patterns. GTH release is masculinized equally well by implants of hormones on either day 2 or day 5. Female sexual behavior is affected only by neonatal implants on day 2. Hormone specificity: Estradiol is as effective as T in masculinizing all three neuroendocrine parameters. In any particular neural site in which T implants produce an alteration in the neuroendocrine response, a similar effect is produced by E 2 implants in the same site. It is suggested that independent masculinization of GTH, female sexual behavior and masculine sexual behavior patterns is produced by the action of T and/or E 2 on separate neural areas, and that these neural areas may be susceptible to the action of hormones at different times.