Testicular hormones are necessary for sexual behaviors in all mammals, including the human. Castration and other means of reducing testicular hormone concentrations always lead to reduced intensity of sexual behavior. This statement does not imply that reduction of blood androgen concentrations to a very low level eliminates sexual behavior in every individual. We have had a few castrated rats that copulated with exactly the same intensity as intact rats for more than 2 months after castration. At sacrifice, their accessory sexual glands were completely atrophied, as is always the case in castrated animals, showing that blood androgen concentration was as much reduced in these animals as it was in the castrated rats that showed no copulatory behavior at all. The proportion of rats maintaining cop-ulatory behavior for a long time in the absence of testicular hormones is well under 1%, at least in my laboratory. This kind of most unusual individual does not in any way contradict the conclusion that sexual behavior is much reduced when androgen concentrations are reduced. They just illustrate a very fundamental principle in medicine, biology, psychology and many other sciences: interindividual variation is considerable and, if we want to come across an exception to a principle, there is always one to find. By the way, the existence of exceptional rats and humans should make us very sceptical to case studies.
Since the main testicular hormone, testosterone, may be reduced to dihydrotestos-terone and aromatized to estradiol, and since both 5a-reductase and aromatase are present at brain sites important for sexual behaviors, it is quite logical to ask whether these products of testosterone metabolism rather than testosterone itself are responsible for the behavioral actions of testicular hormones. As we have seen, there is no unequivocal answer to this question. Among rodents, it appears that both estradiol and consequently estrogen receptors, and dihydrotestosterone, and consequently the androgen receptor, are of importance for normal masculine sexual behavior in some species. However, sexual behaviors can be induced by the exclusive stimulation of androgen receptors in other rodent species. In non-rodent species, the confusion is still more pronounced. Some, like rabbits and rhesus monkeys, do not respond at all to estrogen treatment but respond well to treatment with dihydrotestosterone, showing that androgen receptor stimulation alone is sufficient for male sexual behaviors. Others, like pigs (Levis and Ford, 1989) and rams (D'Occhio et al., 1985), seem to require simultaneous stimulation of androgen and estrogen receptors for the expression of the complete copulatory behavior pattern. The cynomolgus monkey represents a case where no firm conclusion is possible. In the human, we do not have enough data for proposing a definitive hypothesis, but there is no doubt that relevant clinical studies suggest that the androgen receptor alone is involved.
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