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SUMMARY
Male Wistar rats were castrated on the day of birth and divided into two groups; the first was injected with 0·1 mg. testosterone propionate (TP), on the day of castration and the second with 0·5 mg. TP after day 10. When 45 days old, all were grafted with an ovary in the kidney. Animals in the first group showed ovaries with ripening follicles without corpora lutea; those in the second group had corpora lutea at different stages of maturation. Ovaries grafted into female rats spayed on the day of birth developed luteinization even when injected with 0·5 mg. TP after the 10th day of life, but not if the hormone was injected earlier.
Since the hypothalamus is sensitive to androgens only before the 10th day of life even in gonadectomized rats, it can be argued that the female pattern of gonadotrophin control does not correspond to the undifferentiated hypothalamus but depends on some active central mechanism. The period during which the hypothalamus is still sensitive to androgens would correspond to the undifferentiated equipotential stage.
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SUMMARY
A single injection of 20 μg chlorpromazine/g body weight into male rats 10 days after birth accelerated spermatogenesis when the animals were 45 days old; this was not observed in rats injected on days 1, 5, 8, 12 or 15 of life. When half an ovary was grafted into the eye of rats treated on day 10, they showed a higher incidence of luteinization than ovarian grafts in rats treated at any other age. Compared with animals surgically castrated at the same age, chlorpromazine did not act as by 'pharmacological castration', but induced some alteration in the brain which promoted higher secretion of luteinizing hormone, characteristic of the female pattern of gonadotrophin control, as demonstrated by accelerated spermatogenesis and a higher degree of luteinization. These results suggest that the sexual differentiation of the brain occurs on about the 10th day of postnatal life and can be blocked by chlorpromazine.
