Although the dependence of sexual behavior on gonadal hormones has been demonstrated in numerous experiments involving gonadectomy and hormonal replacement, there are very few research data available on the emergence of sexual behavior during spontaneous pubertal development. The most comprehensive studies on lower mammals have been reported by S?dersten and others who assessed sexual behavior and plasma testosterone concentrations in developing normal male rats and tested the effectiveness of various steroid hormone implants in inducing precocious mating behavior in prepubertal males. The results of the first part of the experiment showed no marked changes of testosterone levels in the majority of cases on the day before or after the first mount, intromission, or ejaculation was observed, although it appears from the graphs in their publication that the onset of mating behavior coincided with the beginning of a systematic gradual elevation of plasma testosterone levels. Their finding makes it unlikely that an increase of testosterone production was primarily responsible for the onset of mating behavior. Testosterone treatment, however, of prepubertal rats resulted in precocious onset of mating behavior, as had been shown previously by other authors. To explain the onset of mating behavior in spontaneous puberty without marked changes in testosterone levels, the authors suggested an alteration of the sensitivity of the sex-regulating systems of the central nervous system to testosterone. This hypothesis was supported by the demonstration that castrated immature male rats displayed less sexual behavior than castrated adult male rats without prior sexual experience, although the immature rats were exposed to equal or higher testosterone concentrations. Moreover, the immature males needed more mounts and intromissions prior to ejaculation and displayed longer response latencies which also may be linked to their lower behavioral sensitivity to testosterone. In both groups, higher testosterone levels induced higher levels of sexual performance. The results by S?dersten and others seem to indicate that both increased behavioral sensitivity to testosterone and increased testosterone levels determine the development of sexual behavior during puberty in the male rat. It is conceivable that the increase of behavioral sensitivity to testosterone early in puberty is mediated by LH-RH increases which probably predate the enhancement of gonadal testosterone production. The same reasoning applies to the sensitivity difference between adult and immature rats, since LH-RH production must be assumed to remain elevated above prepubertal levels throughout adulthood.
There are no similarly comprehensive studies on sexual behavior in pubertal primates, but some hormone-behavior correlations have recently been presented by Rose and others. This team followed five adolescent male rhesus monkeys longitudinally from age two through age four with the collection of monthly testosterone levels and observations of behavior. These animals were part of a larger social group of rhesus monkeys of varying ages. Typically, adult rhesus males show strong elevations of both testosterone and sexual behavior during the breeding season and relatively low levels during the remainder of the year. In the adolescent males, testosterone levels showed initial seasonal rises by age three but did not show the adult male seasonal pattern until age four years. Sex behavior demonstrated (gradual) seasonal increases in both year two and three prior to the rise in testosterone. These results appear to be quite similar to the ones in the rat, but whether or not the same explanations apply, needs to be clarified in future investigations. Social learning is an additional potential factor which must be considered in these group-reared animals. Another noteworthy finding by Rose and coworkers was that the extent of the increase of testosterone levels during the third year depended on the number of adult males present in a given social group, probably affecting the relative rank of the adolescents in the dominance hierarchy. Similar delays of pubertal maturation caused by the presence of intact adult males have been described for rodents (e.g., McKinney and Desjardins).
In summary, the animal literature suggests that pubertal rises in male sexual behavior can be caused both by increases in testosterone production and by increased behavioral sensitivity to testosterone. The latter may be due to early LH-RH production or, independently, to CNS maturation. Comparable data on female puberty and sexual behavior have not been described.