Male rats were castrated on the day of birth (day 1) and injected with either testosterone, dihydrotestosterone, a synthetic oestrogen (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 5alpha-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 preinatal 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 5alpha-reduction of unsaturated C19-steriods to dihydrotestosterone in peripheral tissues is also required to complete the development of the male genital tract.
Groups of neonatal female rats were treated for the first 5 days of life with oestradiol-17beta, oestradiol benzoate or a synthetic oestrogen, 11beta-methoxy-17-ethynyl-1,3,5(10)-oestratriene-3,17beta-diol (RU 2858), in daily doses ranging from 0-5 to 1000 ng. Oestradiol-17beta 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.
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.
SUMMARY1. Various methods of stimulating the hypothalamus were applied to the guinea-pig with the aim of inducing ovulation.2. Electrochemical stimulation of the hypothalamus, or gross stimulation of the brain, was ineffective.3. Electrical stimulation of the medial basal hypothalamus or rostral hypothalamus elicited gonadotrophin release.4. Despite variation of the time and intensity of stimulation, follicular luteinization was more common than the formation of new corpora lutea.5. Electrical stimulation of the medial basal hypothalamus often caused luteinization of follicles. Fewer animals responded to excitation of the rostral hypothalamus, but in those that did, ovulation occurred more frequently.6. The present observations contrast markedly with comparable. studies on the rat, where both electrochemical and electrical stimulation of the hypothalamus readily induce ovulation.
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