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SUMMARY
Male rats were castrated on the day of birth (day 1) and injected with either testosterone, dihydrotestosterone, a synthetic oestrogen (RU 2858), RU 2858 + dihydrotestosterone, or oil from days 1 to 5. The aromatizable androgen, testosterone, and RU 2858 suppressed both cyclic gonadotrophin secretion, indicated by the absence of corpora lutea from implanted ovarian grafts, and the behavioural response to oestradiol benzoate + progesterone injections in adulthood. The 5α-reduced androgen, dihydrotestosterone alone did not affect gonadotrophin secretion or female receptive behaviour, but like testosterone, it increased penis development in response to testosterone propionate, and this was positively correlated with copulatory efficiency, i.e. the ratio of intromission to mount frequencies. Nevertheless, ejaculation only occurred among animals that had received testosterone or RU 2858 + dihydrotestosterone. The results support the concept that during the perinatal period, neural conversion of androgens to oestrogens is important both for the suppression of female gonadotrophin secretion and behaviour patterns as well as for the organization of male behaviour patterns. The 5α-reduction of unsaturated C19-steroids to dihydrotestosterone in peripheral tissues is also required to complete the development of the male genital tract.
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Department of Physiology, Royal Veterinary College, Royal College Street, London, NW1 OTU
(Received 19 February 1976)
Administration of testosterone to newborn female rats suppresses cyclic gonadotrophin secretion and sexual receptivity in adulthood (Barraclough, 1961). This effect probably depends upon the conversion of testosterone to oestrogen in the brain (Reddy, Naftolin & Ryan, 1974; Doughty, Booth, McDonald & Parrott, 1975). Hydroxylation of the androgen molecule at carbon-19 is the initial step in aromatization (Gual, Morato, Hayano, Gut & Dorfman, 1962), and injecting 19-hydroxytestosterone (17β-hydroxy-4-androsten-19-ol-3-one; 19HT) into neonatal female rats prevents cyclic ovulation in adulthood (McDonald & Doughty, 1974). On the other hand, 5α-reduction of testosterone blocks conversion to oestrogen as the product, dihydrotestosterone (17β-hydroxy-5α-androstan-3-one; DHT), cannot be aromatized. Since DHT does not affect sexual differentiation of the brain (McDonald & Doughty, 1974), the non-aromatizable 5α-reduced form of 19HT (17β-hydroxy-5α-androstan-19-ol-3-one; 5α-19HT) should similarly be ineffective. This study compares the defeminization induced in
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Groups of rats were castrated on the day of birth (day 1) and injected with testosterone, androst-4-ene-3,6,17-trione (ADT, an inhibitor of aromatization), testosterone + ADT or oil daily from day 1 to day 5. The aromatizable androgen testosterone suppressed both cyclic gonadotrophin secretion, as judged from the absence of corpora lutea in grafted ovaries, and the behavioural response to injections of oestradiol benzoate and progesterone in adulthood. It also stimulated normal development of the penis and ejaculation in behaviour tests carried out after injections of testosterone propionate. The aromatization inhibitor ADT, like oil, did not affect either cyclic gonadotrophin secretion or receptive behaviour, but injections of ADT given at the same time as testosterone significantly reduced the effects of the androgen on both cyclic gonadotrophin secretion and receptive behaviour. Although neonatal administration of ADT did not affect the testosterone-stimulated development of the penis or the ability of the rats to achieve penile intromissions, it did interfere with ejaculation. None of the rats which had been injected with testosterone+ADT ejaculated. These results support the concept that during infancy neural conversion of androgens to oestrogens is important both for the suppression of the female patterns of gonadotrophin secretion and sexual behaviour and for the central organization of normal patterns of male sexual behaviour. Normal completion of the differentiation of the male genital tract appears to be independent of the central organization of masculine patterns of sexual behaviour.
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SUMMARY
In the guinea-pig, when bilateral oestrogen implants were placed in the medial basal hypothalamus, anterior hypothalamus or suprachiasmatic area on day 10 of the oestrous cycle, ovarian changes indicative of gonadotrophin secretion were observed on day 15. Similarly located cholesterol implants and oestrogen implants outside this region were without effect. The gonadotrophin release was likely to have been induced by an action of the steroid at the hypothalamic, rather than the pituitary level, since bilateral implants of oestrogen in the pars distalis caused ovarian activation in only one out of eight animals. Signs of normal ovulation were evident in only three out of 19 animals in which oestrogen was implanted in the medial basal hypothalamus on day 10 and left in place for 10 days. The ovaries of some other animals bore the traces of luteal bodies formed in response to the initial exposure to oestrogen; other ovaries contained only large healthy or atretic follicles and spontaneous ovulation was apparently blocked. It is concluded that exposure of the hypothalamo-hypophysial system of the guinea-pig to an increased amount of oestrogen initially stimulates and then inhibits ovulatory gonadotrophin secretion. Tonic gonadotrophin secretion is unaffected.
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SUMMARY
Groups of neonatal female rats were treated for the first 5 days of life with oestradiol-17β, oestradiol benzoate or a synthetic oestrogen, 11β-methoxy-17-ethynyl-1,3,5(10)-oestratriene-3,17β-diol (RU 2858), in daily doses ranging from 0·5 to 1000 ng. Oestradiol-17β had no effect on adult ovarian cyclicity or sexual receptivity after ovariectomy and oestrogen + progesterone treatment. Ovarian cyclicity was prevented by 100 ng or more oestradiol benzoate/day, and by all doses of RU 2858. Only rats receiving 50 ng oestradiol benzoate/ day or 0·5 ng RU 2858/day showed normal receptivity. The defeminizing action of RU 2858 was at least 100 times greater than that of oestradiol benzoate; it is suggested that this greater potency is due to the low affinity of RU 2858 for the oestradiol-binding protein in the plasma of neonatal rats. These results indicate that defeminization of the neonatal rat brain can be induced by physiological amounts of oestrogen, and are discussed with reference to the action of testosterone.
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Department of Physiology, The Royal Veterinary College, Royal College Street, London, NW1 OTU
(Received 24 March 1975)
Neonatal treatment of female rats with testosterone will prevent the cyclic pattern of gonadotrophin secretion and sexual receptivity in adulthood (Barraclough, 1961). This effect probably depends on the production of small amounts of oestrogen from testosterone in the brain (Reddy, Naftolin & Ryan, 1974) since non-aromatizable androgens do not have this effect (McDonald & Doughty, 1974). Antagonism of testosterone-induced masculinization by the anti-oestrogen MER-25 (ethamoxytriphetol; McDonald & Doughty, 1973/74; Doughty & McDonald, 1974) supports this hypothesis. Neonatal treatment with very low doses of the synthetic oestrogen RU 2858 (11β-methoxy-17-ethynyl-1,3,5,(10)-oestratriene-3,17β-diol) will also defeminize the female brain (Doughty, Booth, McDonald & Parrott, 1975). The object of this study was to prevent defeminization, induced by neonatal treatment with RU 2858, with the anti-oestrogen MER-25.
Starting within 24 h of birth (day 1) and continuing for 5
