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Prenatal treatment of male rats with the anti-androgen, flutamide (FL), demasculinizes the sexually dimorphic spinal nucleus of the bulbocavernosus (SNB) by reducing the number of SNB neurons, the size of the somas and nuclei of SNB neurons, and the size of their target muscles in adulthood. However, FL does not affect mounting or the traditional, postural measure of intromission, indicating that the SNB system does not play a major role in the mediation of these particular behaviors. Postnatal testosterone propionate (TP) treatment of male rats castrated on the day of birth results in more male copulatory behaviors in adulthood and masculinizes all measures of the SNB system. The postnatal masculinization by TP is more pronounced in males treated prenatally with FL, for morphological but not behavioral measures. The combined treatment of prenatal FL and day 1 castration without TP therapy results in a male with a completely demasculinized SNB system. Specifically, such males have SNB neurons that are as scarce and as small as those of females and, like females, they lack the target muscles of the SNB. These results support the hypothesis that perinatal androgens normally direct the sexually dimorphic development of the SNB and its target muscles.

the journal of neuroscience/the journal of neuroscience

Hormonal control of a developing neuromuscular system. I. Complete Demasculinization of the male rat spinal nucleus of the bulbocavernosus using the anti-androgen flutamide