Exogenous androgen during development alters adult partner preference and mating behavior in gonadally intact male rats

Abstract

In the rat, neonatal administration of testosterone propionate to a castrated male causes masculinization of behavior. However, if an intact male is treated neonatally with testosterone (hyper-androgen condition), male sexual behavior in adulthood is disrupted. There is a possibility that the hyper-androgen treatment is suppressing male sexual behavior by altering the male’s partner preference and thereby reducing his motivation to approach the female. If so, this would suggest that exposure to supra-physiological levels of androgen during development may result in the development of male-oriented partner preference in the male. To test this idea, male rats were treated either postnatally or prenatally with testosterone, and partner preference and sexual behavior were examined in adulthood. The principal finding of this study was that increased levels of testosterone during early postnatal life, but not prenatal, decreased male sexual behavior and increased the amount of time a male spent with a stimulus male, without affecting the amount of time spent with a stimulus female during partner preference tests. Thus, the reduction in male sexual behavior produced by early exposure to high levels of testosterone is not likely due to a reduction in the male’s motivation to approach a receptive female.

Prenatal testosterone supplementation alters puberty onset, aggressive behavior, and partner preference in adult male rats

“…Despite this, animals treated prenatally with T were efficient in carrying out typical male sexual behavior and were efficient at producing descendants; females rats mated with males of the testosterone group had normal pregnancies and, as consequence, fertility was normal. These results indicate that supra-physiological levels of testosterone administered prenatally do not significantly alter male behavior [36], in contrast with results obtained by others when the hormonal manipulations occurred during the postnatal period [5,36]; thus prenatal exposure to T did not reduce motivation to approach a female [36]. Additionally, the unaltered gestational index suggests that testosterone supplementation was not toxic to the fetuses; for all pregnant females, termination revealed all fetuses were alive [25].…”

“…In a study performed by Henly et al [36], who used similar procedures to evaluate sexual behavior and sexual preference, no differences were found. An important difference between these experiments was the dose of TP and the period of treatment; in our study we used 1 mg/ animal/day on GD 17,18,and 19 whereas Henly et al [36] used 2 mg/0.1 ml/day on GD 16,17,18,19,and 20. Also in this study, males treated with TP from the day of birth through PND 21 and tested as intact adults spent more time with a sexually active male than with control males.…”

Neonatal agonism of ERβ impairs male reproductive behavior and attractiveness

“…Further studies using additional doses of DPN and PPT, as well as antagonists for ERα and ERβ would be required to further elucidate these interactions. Moreover, prior work has established that although postnatal administration of testosterone to neonatal castrates can rescue male sexual behavior, exogenous administration to gonadally intact neonates results in compromised male sexual performance (Henley et al, 2010; Pollak and Sachs, 1975; Zadina et al, 1979). Thus there appears to be an “optimal range” in which steroid hormones induce masculinization, and doses above or below that range can result in partial demasculinization.…”

Long-term under-masculinization in male rabbits due to maternal stress is reversed by prenatal administration of testosterone

“…Whereas in some mammalian studies, prenatal treatment with T had no effect on male AGD or weight at birth or adulthood (Dela Cruz and Pereira, 2012;Keisler et al, 1991;vom Saal, 1979), in other studies it had (Gill and Hosking, 1995;Juárez et al, 1995;Manikkam et al, 2004). Furthermore and somewhat paradoxically, in rats prenatal treatment resulted in no effect on or decreased AGD (Dela Cruz and Pereira, 2012;Hotchkiss et al, 2007;Tehrani et al, 2013;Wolf et al, 2002) and in delayed puberty, but increased aggression, altered sexual preference and increased vocalization (Henley et al, 2010;Hotchkiss et al, 2007;Juárez et al, 1995;Kršková and Talarovičová, 2005).…”