Search Results
Search for other papers by H. F. URBANSKI in
Google Scholar
PubMed
Search for other papers by B. K. FOLLETT in
Google Scholar
PubMed
Plasma levels of LH are generally higher in male than in female quail. This dimorphism was found to persist in quail which had been through a breeding cycle and then gonadectomized. Under long daylengths (12 h light: 12 h darkness (12L : 12D) or 16L : 8D) ovariectomized quail had plasma levels of LH that were 55–70% of those seen in castrated birds. The difference was reduced after transfer to short days (8L : 16D) when LH concentrations fell to basal levels, but again became more pronounced when the quail were restimulated with long photoperiods. Thus, the photoperiodic response system is sexually differentiated.
Search for other papers by A. Perakis in
Google Scholar
PubMed
Search for other papers by F. Stylianopoulou in
Google Scholar
PubMed
ABSTRACT
Exposure of the developing female brain to a 5α-dihydrotestosterone surge on day 18 of gestation resulted in defeminization and slight masculinization of the brain. In contrast, abolition of the androgenic effects of the testosterone peak naturally occurring in male fetuses on day 18 of gestation by exposure of the developing male brain to cyproterone acetate, at that time, resulted in demasculinization while feminization was not affected. On the basis of these results, we suggest that both the prenatal testosterone peak and the high testosterone levels occurring in males neonatally are necessary for aromatization sufficient to effect complete male rat brain sexual differentiation.
J. Endocr. (1986) 108, 281–285
Search for other papers by F. GOGAN in
Google Scholar
PubMed
Search for other papers by A. SLAMA in
Google Scholar
PubMed
Search for other papers by B. BIZZINI-KOUTZNETZOVA in
Google Scholar
PubMed
Search for other papers by F. DRAY in
Google Scholar
PubMed
Search for other papers by C. KORDON in
Google Scholar
PubMed
Testosterone secretion in the male rat was high during the late fetal and immediate postnatal periods. It then showed a rapid decrease 3 h after birth and remained low until puberty.
Male rats from mothers given daily injections of an antibody to testosterone during the week before delivery displayed an LH peak when they were adult, orchidectomized and implanted with oestradiol. However, the amplitude of the peak was far smaller than in female rats from the same mothers treated in the same manner.
Thus, the critical period during which testosterone triggers hypothalamic sexual differentiation is very close to birth, possibly starting at the end of the fetal period.
Search for other papers by JANET E. BOOTH in
Google Scholar
PubMed
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
Search for other papers by S. F. Pang in
Google Scholar
PubMed
Search for other papers by F. Tang in
Google Scholar
PubMed
ABSTRACT
Male and female mice and hamsters were decapitated 1–5 days after birth and serum concentrations of testosterone determined by radioimmunoassay. In the two species studied, serum levels of testosterone in male pups were significantly (P <0·05) higher than those obtained in female neonates. This lends support to the hypothesis that circulating levels of testosterone play an important role in the process of neural sexual differentiation in rodents. Moreover, the sex differences in serum concentrations of testosterone in neonatal rodents together with the detectable levels of testosterone in female neonates may suggest that androgenization is a dose-dependent phenomenon. Alternatively, they may indicate that a minimum concentration of the steroid must be present for androgenization to occur during the critical period of neural sexual differentiation and that this 'threshold' is exceeded in male but not in female rodents.
J. Endocr. (1984) 100, 7–11
Search for other papers by J. Klindt in
Google Scholar
PubMed
Search for other papers by J. J. Ford in
Google Scholar
PubMed
Search for other papers by G. J. Macdonald in
Google Scholar
PubMed
ABSTRACT
The effect of testosterone propionate (TP), alone and in combination with porcine GH, on the growth of hypophysectomized rats was investigated. An initial study determined doses of TP and GH which would result in a synergistic response. Hypophysectomized male rats, approximately 40 days of age, received GH at doses of 5, 25 and 62·5 μg/day administered in two injections/day at 08.00 and 16.00 h. At all doses of GH, administration of TP at 100 μg/day significantly enhanced the GH-stimulated rate of growth. This growth enhancement by TP was greatest in combination with GH at 25 μg/day. In a subsequent study, growth responses to 25 μg GH/day and 100 μg TP/day were examined in animals with differing degrees of sexual differentiation. Sex groups were: intact males, males castrated at 11 days of age and females administered 100 μg TP at 3 days of age (masculinized rats), and males castrated at 2 days of age and normal females (non-masculinized rats). In all sex groups, growth of hypophysectomized rats was stimulated by GH. Genetic sex and masculinization did not influence the response to GH. Masculinized hypophysectomized rats exhibited significantly greater rates of growth and final live, empty body, liver and kidney weights than non-masculinized hypophysectomized rats. All sex groups other than normal females responded synergistically to the combination treatment of GH plus TP. Rats that experienced neonatal exposure to testosterone became programmed to respond to testosterone and demonstrated greater rates of growth and body and organ weights when administered the combination of GH plus TP. These data indicate that TP synergizes with GH to promote growth of hypophysectomized rats appropriately programmed to respond. The ability to manifest a synergistic response is a differentiated trait dependent upon exposure to testosterone during the appropriate period of development. The time of differentiation of this ability to respond to testosterone occurs earlier than that for differentiation of body growth.
Journal of Endocrinology (1990) 127, 249–256
Search for other papers by F. SASAKI in
Google Scholar
PubMed
Search for other papers by M. SANO in
Google Scholar
PubMed
To clarify the role of the ovary in the sexual differentiation of prolactin and growth hormone cells, the anterior pituitary glands of mice ovariectomized before or after puberty were studied by a stereological morphometric technique with the electron microscope. A marked sex difference was observed in the relative proportions of these two types of cells in normal adult control animals. In male mice about 52% of anterior pituitary cells were growth hormone cells and about 10% were prolactin cells, while in female mice prolactin cells represented about 39% and growth hormone cells about 37% of the anterior pituitary cell population. Ovariectomy before puberty reduced the proportion of prolactin cells to about 10% and increased growth hormone cells to about 50% of the cell population. The size of prolactin cells and the development of their cell organelles was also reduced. Ovariectomy after puberty had less marked effects. These results suggest that ovariectomy before puberty induced the male phenotype by inhibition of the differentiation of prolactin cells and stimulation of the differentiation of growth hormone cells. The significance of these results in relation to the sexual differentiation of the pituitary gland is discussed.
Search for other papers by JANET E. BOOTH in
Google Scholar
PubMed
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.
Search for other papers by F. Sasaki in
Google Scholar
PubMed
Search for other papers by M. Sano in
Google Scholar
PubMed
To study the effect of the ovary on sexual differentiation of somatotrophs and lactotrophs, the anterior pituitary glands of castrated adult male mice which had received an ovarian transplant during postnatal development were studied using a stereological morphometric technique with an electron microscope. In adult male mice which were castrated neonatally and given ovarian transplants at the age of puberty (NCT-males), the ovaries contained follicles and corpora lutea. The percentages (∼40) and numbers (∼2 × 105) of lactotrophs were similar in normal dioestrous females and NCT-males, but were higher than the percentage (9·3) and number (4·6 × 104) in normal males. Ovarian grafts in adult male mice which were simultaneously castrated and given an ovarian transplant just before puberty (PCT-males) contained numerous follicles of various sizes but no corpora lutea. The percentage (46·8) and number (3·9 × 105) of lactotrophs were greater in these mice than in dioestrous females. The percentage of somatotrophs in NCT-males (34·7) was less than in normal males (52·6), but was similar to that in dioestrous female mice (37·4). The percentage of somatotrophs in PCT-males (27·4) was less than in normal male and dioestrous female mice. These data indicate that lactotrophs and somatotrophs differentiate to the female phenotype when a cyclically functional ovary is present after puberty.
Search for other papers by I. J. CLARKE in
Google Scholar
PubMed
Search for other papers by R. J. SCARAMUZZI in
Google Scholar
PubMed
Search for other papers by R. V. SHORT in
Google Scholar
PubMed
M.R.C. Unit of Reproductive Biology, 2 Forrest Road, Edinburgh, EH1 2QW
(Received 11 June 1976)
Testosterone treatment of female mammals during a critical period of foetal or neonatal life affects their postpubertal endocrine and behavioural activity. For example, it prevents the occurrence of regular ovulatory cycles in adult rats (Barraclough & Gorski, 1961), guinea-pigs (Brown-Grant & Sherwood, 1971), hamsters (Swanson & Brayshaw, 1973) and sheep (Short, 1974), which is apparently due to a failure of oestrogen to facilitate the release of luteinizing hormone (positive feedback) (Brown-Grant, 1974; Short, 1974). Positive feedback is a sexually dimorphic character in sheep and is only shown by ewes (Short, 1974; Karsch & Foster, 1975). Female sheep foetuses exposed to testosterone from days 20 or 60 of gestation until birth not only failed to show positive feedback (Short, 1974), but were incapable of displaying behavioural oestrus, even when given 800 μg oestradiol benzoate (OB) (I.
