Hormonal modulation of genital reflexes in male and masculinized female dogs

When testosterone propionate (TP) is administered to adult, neonatally castrated male dogs and to adult females with masculinized genitalia produced by prenatal and neonatal exposure to androgen, both types of animals are unsuccessful in their attempts to copulate with receptive females. They mount and thrust vigorously but do not achieve intromission and establish a copulatory "lock." The deficit could be due to incomplete "organization" of neuromuscular mechanisms mediating erection or to the fact that the penis of such dogs are abnormally short. In this experiment, neonatally castrated males and genitally masculinized females were tested before and after TP treatment for responses to manual stimulation of the genitalia. An additional experimental group consisted of males castrated as adults, and there was a control group of normal males. After a series of TP injections, neonatally castrated males, adult castrates, and genitally masculinized females exhibited complete and strong erectile and ejaculatory reflexes. Erect penis lengths of neonatally castrated males and masculinized females were significantly shorter than those of normal males or of males castrated as adults. It is tentatively concluded that the failure of males castrated at birth, and of genitally masculinized females, to insert and lock when mounting receptive females is due to incomplete penile development and not to incomplete "organization" of spinal reflex mechanisms. However, because artificial stimulation was employed, results of this study do not prove that central nervous system mechanisms necessary for insertion and locking in copula were normally developed.