Prevention of Central Defeminization but Not Masculinization in Male Rats by Inhibition Neonatally of Oestrogen Biosynthesis

Vreeburg, J. T. M.; Vaart, P. D. M. van der; Schoot, P. van der

doi:10.1677/joe.0.0740375

Cited by 146 publications

(60 citation statements)

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“…That there is a difference in effect between rats and humans is hardly surprising, in view of the gross differences in behaviors observed, time courses of perinatal hormone administration and of developmental sequences, and the particular steroids administered. The relative vulnerability of masculine and feminine behavior patterns to neonatally administered progesterone in this study is, however, somewhat surprising in light of reports that neonatal treatment of intact males with an aromatase inhibitor (which blocks conversion of androgens to estrogens) enhanced the display of feminine behavior but did not affect masculine behavior of rats [5,23]. On the other hand, administration of an aromatase inhibitor together with testosterone to neonatally castrated rats suppressed both masculinization and defeminization [2].…”

Section: Discussioncontrasting

confidence: 66%

Effects of neonatal exposure to progesterone on sexual behavior of male and female rats

Hull

1981

Physiology & Behavior

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Section: Discussioncontrasting

confidence: 66%

Effects of neonatal exposure to progesterone on sexual behavior of male and female rats

Hull

1981

Physiology & Behavior

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“…Dihydrotestosterone (a non-aromatizable androgen) is unable to affect reproductive function (Whalen & Luttge 1971, McDonald & Doughty 1972, 1974, and the effects of testosterone were blocked by inhibitors of aromatization (Vreeburg et al 1977) and antioestrogens (McDonald & Doughty 1972). The analysis of the effects of combined administration of testosterone and oestradiol with raloxifene supports the oestrogenic activity of raloxifene.…”

Section: Discussionmentioning

confidence: 95%

Comparative effects of testosterone propionate, oestradiol benzoate, ICI 182,780, tamoxifen and raloxifene on hypothalamic differentiation in the female rat

Pinilla¹,

Barreiro²,

Gonzalez³

et al. 2002

Journal of Endocrinology

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Hypothalamic differentiation in the female rat during the neonatal period is critically dependent on the steroid milieu, as permanent changes in reproductive function are observed after administration of oestradiol and testosterone during such a critical stage. Selective oestrogen modulators (SERMs) constitute a family of drugs that, depending on the tissue, are able to exert oestrogenic or antioestrogenic actions. The present experiments were conducted to analyse whether the SERMs, tamoxifen and raloxifene, can cause oestrogenic actions during the hypothalamic differentiation period.Postnatal female rats were injected between days 1 and 5 with 100 µg/day tamoxifen, raloxifene or ICI 182,780 (a pure antioestrogen). Other groups of animals were injected on day 1 of age with 100 µg oestradiol benzoate (OeB) or 1·25 mg testosterone propionate (TP) alone or in combination with raloxifene (500 µg/day between days 1 and 5). In all experimental groups, the age, body weight and concentrations of serum gonadotrophins at vaginal opening were recorded, whereas vaginal cyclicity and the negative and positive feedback between oestradiol and LH were monitored in adulthood.The results obtained confirmed the ability of high doses of OeB or TP to alter the normal differentiation of the brain permanently. They also reinforced the hypothesis that oestrogens are also necessary for normal brain differentiation in female rats because administration of a pure antioestrogen, such as ICI 182,780 permanently altered the function of the reproductive axis. In addition, our data provided evidence for different actions of the two SERMs under analysis (raloxifene and tamoxifen) upon peripheral targets, as raloxifene advanced vaginal opening whereas tamoxifen did not. In contrast, their actions on brain differentiation appeared similar and analogous to those obtained after neonatal administration of oestradiol, as evidenced by vaginal acyclicity, ovarian atrophy, sterility and abolition of negative and positive feedback between oestradiol and LH, thus suggesting an oestrogenic action of these SERMs on hypothalamic differentiation. Moreover, the oestrogenic activity of raloxifene was supported by its inability to block the effects of OeB and TP administered neonatally.In conclusion, the present results indicated that the SERMs, tamoxifen and raloxifene, exert an oestrogen-like effect upon hypothalamic differentiation of the neonatal female rat.

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“…For the rabbit, data represent means Ϯ SEM; for the ferret, individual profiles of LH release following mating in a representative male and female tested while in breeding condition. male rat's hypothalamus (161,220,226). However, the site and mechanism by which testosterone acts to masculinize the neuroendocrine circuitry controlling GnRH release in males is unclear.…”

Section: Figmentioning

confidence: 99%

“…BAKKER AND BAUM male rat's hypothalamus (161,220,226). However, the site and mechanism by which testosterone acts to masculinize the neuroendocrine circuitry controlling GnRH release in males is unclear.…”

mentioning

confidence: 99%

Neuroendocrine Regulation of GnRH Release in Induced Ovulators

Bakker

Baum

2000

Frontiers in Neuroendocrinology

180

135

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GnRH is the key neuropeptide controlling reproductive function in all vertebrate species. Two different neuroendocrine mechanisms have evolved among female mammals to regulate the mediobasal hypothalamic (MBH) release of GnRH leading to the preovulatory secretion of LH by the anterior pituitary gland. In females of spontaneously ovulating species, including rats, mice, guinea pigs, sheep, monkeys, and women, ovarian steroids secreted by maturing ovarian follicles induce a pulsatile pattern of GnRH release in the median eminence that, in turn, stimulates a preovulatory LH surge. In females of induced ovulating species, including rabbits, ferrets, cats, and camels, the preovulatory release of GnRH, and the resultant preovulatory LH surge, is induced by the receipt of genital somatosensory stimuli during mating. Induced ovulators generally do not show "spontaneous" steroid-induced LH surges during their reproductive cycles, suggesting that the positive feedback actions of steroid hormones on GnRH release are reduced or absent in these species. By contrast, mating-induced preovulatory surges occasionally occur in some spontaneously ovulating species. Most research in the field of GnRH neurobiology has been performed using spontaneous ovulators including rat, guinea pig, sheep, and rhesus monkey. This review summarizes the literature concerning the neuroendocrine mechanisms controlling GnRH biosynthesis and release in females of several induced ovulating species, and whenever possible it contrasts the results with those obtained for spontaneously ovulating species. It also considers the adaptive, evolutionary benefits and disadvantages of each type of ovulatory control mechanism. In females of induced ovulating species estradiol acts in the brain to induce aspects of proceptive and receptive sexual behavior. The primary mechanism involved in the preovulatory release of GnRH among induced ovulators involves the activation of midbrain and brainstem noradrenergic neurons in response to genital-somatosensory signals generated by receipt of an intromission from a male during mating. These noradrenergic neurons project to the MBH and, when activated, promote the release of GnRH from nerve terminals in the median eminence. In contrast to spontaneous ovulators, there is little evidence that endogenous opioid peptides normally inhibit MBH GnRH release among induced ovulators. Instead, the neural signals that induce a preovulatory LH surge in these species seem to be primarily excitatory. A complete understanding of the neuroendocrine control of ovulation will only be achieved in the future by comparative studies of several animal model systems in which mating-induced as well as spontaneous, hormonally stimulated activation of GnRH neurons drives the preovulatory LH surge. KEY WORDS: GnRH; MBH; induced ovulators; neuroendocrine regulation; preovulatory LH surge; spontaneous ovulators. © 2000 Academic Press Address correspondence and reprint requests to M. J. Baum at Dept. Biology, Boston University, 5 Cummington Street, Boston...

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Prevention of Central Defeminization but Not Masculinization in Male Rats by Inhibition Neonatally of Oestrogen Biosynthesis

Cited by 146 publications

References 19 publications

Effects of neonatal exposure to progesterone on sexual behavior of male and female rats

Effects of neonatal exposure to progesterone on sexual behavior of male and female rats

Comparative effects of testosterone propionate, oestradiol benzoate, ICI 182,780, tamoxifen and raloxifene on hypothalamic differentiation in the female rat

Neuroendocrine Regulation of GnRH Release in Induced Ovulators

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