The influence of gonadectomy, androgen exposure, or a gonadal graft in the neonatal rat on the volume of the sexually dimorphic nucleus of the preoptic area

Jacobson, CD; Csernus, V.; Je, Shryne; Gorski, RA

doi:10.1523/jneurosci.01-10-01142.1981

Cited by 196 publications

(70 citation statements)

References 14 publications

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“…The developing SDN-POA size, like that of the AVPV, is organized by endogenous gonadal steroid hormones [66]. More specifically, testosterone given to fetal rats on gestational days 18, 19 or 20 (but not earlier in gestation) or on postnatal days 2, 3, 4 or 5 resulted in a larger SDN-POA of females (i.e., masculinized; [125,126]), and deprivation of endogenous hormones via neonatal castration (day 1) in male rats caused the SDN-POA to be smaller, suggesting a feminizing or demasculinizing event [81].…”

Section: Sexually Dimorphic Nucleus Of the Preoptic Area (Sdn-poa)mentioning

confidence: 99%

Developmental programming and endocrine disruptor effects on reproductive neuroendocrine systems

Gore¹

2008

Frontiers in Neuroendocrinology

230

122

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The ability of a species to reproduce successfully requires the careful orchestration of developmental processes during critical time points, particularly the late embryonic and early postnatal periods. This article begins with a brief presentation of the evidence for how gonadal steroid hormones exert these imprinting effects upon the morphology of sexually differentiated hypothalamic brain regions, the mechanisms underlying these effects, and their implications in adulthood. Then, I review the evidence that aberrant exposure to hormonally-active substances such as exogenous endocrine-disrupting chemicals (EDCs), may result in improper hypothalamic programming, thereby decreasing reproductive success in adulthood. The field of endocrine disruption has shed new light on the discipline of basic reproductive neuroendocrinology through studies on how early life exposures to EDCs may alter gene expression via non-genomic, epigenetic mechanisms, including DNA methylation and histone acetylation. Importantly, these effects may be transmitted to future generations if the germline is affected via transgenerational, epigenetic actions. By understanding the mechanisms by which natural hormones and xenobiotics affect reproductive neuroendocrine systems, we will gain a better understanding of normal developmental processes, as well as to develop the potential ability to intervene when development is disrupted.

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Section: Sexually Dimorphic Nucleus Of the Preoptic Area (Sdn-poa)mentioning

confidence: 99%

Developmental programming and endocrine disruptor effects on reproductive neuroendocrine systems

Gore¹

2008

Frontiers in Neuroendocrinology

230

122

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“…In the adult rat, the volume of the SDN-POA is determined by the perinatal action of androgens. 21,22,23,30,32 Jacobson et al 31 have found that gonadectomized and adrenalectomized male rats showed a higher percentage of radioactively labeled cells in the SDN-POA following exposure to [ 3 H]testosterone than gonadectomized and adrenalectomized females. 31 This sex difference might be due to a difference in AR levels in the mPOA.…”

Section: Androgen Receptor Immunoreactivitymentioning

confidence: 99%

Quantitative estimation of estrogen and androgen receptor-immunoreactive cells in the forebrain of neonatally estrogen-deprived male rats

et al. 1997

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Abstract--Using quantitative immunocytochemical procedures, the total number of estrogen and androgen receptors was estimated in a large number of hypothalamic and limbic nuclei of male rats, in which brain estrogen formation was inhibited neonatally by treatment with the aromatase inhibitor 1,4,6-androstatriene-3,17-dione. The highest densities of estrogen receptor immunoreactivity were observed in the periventricular preoptic area and the medial preoptic area. Neonatally estrogen-deprived males showed a higher estrogen receptor immunoreactivity than control males in the periventricular preoptic area and the ventrolateral portion of the ventromedial nucleus of the hypothalamus, i.e. those brain areas in which sex differences have been reported, with female rats showing a greater estrogen binding capacity than male rats. The highest densities of androgen receptor immunoreactivity were found in the septohypothalamic nucleus, the medial preoptic area, the posterior division of the bed nucleus of the stria terminalis and the posterodorsal division of the medial amygdaloid nucleus. No significant differences in distribution or total numbers of androgen receptors were found between neonatally estrogen-deprived males and control males.These findings suggest that neonatal estrogens, derived from the neural aromatization of testosterone, are involved in the sexual differentiation of the estrogen receptor system in the periventricular preoptic area and the ventromedial hypothalamus. The role of neonatal estrogens in the development of the forebrain androgen receptor system is less clear. 1997 IBRO. Published by Elsevier Science Ltd.Key words: neonatal ATD treatment, androgen receptor, estrogen receptor, estrogens, hypothalamus, preoptic area.In mammals, testosterone and estradiol derived from neural aromatization of testosterone act synergistically in the developing male brain to organize its structures and functions, i.e. to masculinize and defeminize the neural substrates that later control sexual behavior and neuroendocrine function. In the rat brain, masculinization results in the display of male-typical sexual behavior (mounts, intromissions and ejaculations) in adulthood. Defeminization results in a loss of cyclic release of gonadotropins necessary for ovulation and a loss of female-typical sexual behavior (lordosis, presenting, ear wiggling, hop and dart) in adulthood (e.g., Ref. 37). Thus, gonadally intact male rats display the complete pattern of male coital behavior when pair tested with an estrous female and no female-typical sexual behavior when pair tested with a sexually active male. However, lordosis behavior can be induced in castrated male rats by administering estradiol and progesterone, although the behavior displayed is usually less intense than that of females, and considerably more estradiol is required for its stimulation. 20,42,54 The development of the female rat brain is generally believed to proceed in the absence of testosterone and estradiol. Gonadally intact female rats display periods of be...

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“…A striking sexual dimorphism in gross morphology of the medial preoptic area (sexually dimorphic nucleus of the preoptic area: SDN-POA) has been recognized in the rat brain 14 . The development of this nucleus starts during late fetal life and depends on the hormonal environment at the critical period of sexual differentiation [14][15][16] . In genetic males, the relatively high levels of perinatal testosterone are aromatized to estradiol in the nervous cells of SDN-POA and the estrogenic signals may be directly responsible for the increase of SDN-POA volume.…”

Section: Development Of the Female Genital Organs And Profile Of Hormmentioning

confidence: 99%

Toxicologic/carcinogenic Effects of Endocrine Disrupting Chemicals on the Female Genital Organs of Rodents

et al. 2004

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Toxicologic/carcinogenic effects of some representative endocrine disrupting chemicals (EDCs) having estrogenic activity, such as alkylphenols, on the female genital organs of rodents, especially rats, are reviewed and discussed, focusing on our recent research. Neonatal treatment of high-dose p-tert octylphenol (t-OP, 100 mg/kg s.c. injection every other day from postnatal day 1 (PND 1) to PND 15) induced various long-term persistent irreversible effects on the female reproductive system of Donryu rats, such as lower gonadotropin levels at prepuberty, inhibition of uterine gland genesis, persistent estrus and polycystic ovaries. The result indicates that neonatal high-dose treatment of estrogenic EDCs can affect gonadotropin secretion during the developmental period of sexual maturation with direct masculinization of the hypothalamic function. Exposure limited to the first 5 days after birth (PNDs 1-5) to 100 mg/ kg t-OP, however, caused delayed influence which was characterized by accerelated appearance of atrophic ovary, manifested by early-occurring and long-term continuing persistent estrus after puberty, whereas no abnormalities could be found with regard to growth and differentiation of the reproductive organs and the hypothalamo-pituitary-gonadal control system up to maturation, the influence being caused by delayed modulation of the hypothalamo-pituitary-gonadal control system. The most notable effect on the female reproductive system when normal cycling rats were exposed to high-doses t-OP for 28 days, was disappearance of the estrous cycle, but no clear changes were detected in other parameters such as uterine weight and morphology. These results indicate that the most serious issue with EDCs is the potential effects of prenatal and/or neonatal exposure on rodents. Well or moderately differentiated adenocarcinomas increased in Donryu rats initiated with N-ethyl-N'-nitro-N-nitrosoguanidine, when high-dose t-OP was given subcutaneously during adulthood. Neonatal exposure for PNDs 1-5 to high-dose t-OP also showed promoting effects on uterine adenocarcinoma development. However, in rats given t-OP for PNDs 1-15, uterine tumor malignancy was clearly increased, although there was no significant alteration in the total incidence of adenocarcinomas. The results are very interesting in consideration of the histogenesis of uterine adenocarcinomas. However, maternal exposure to low doses of EDCs such as nonylphenol and bisphenol A at actual human exposure levels by the oral route showed no effects on growth and development of the female reproductive system or uterine carcinogenesis. These results indicate that dietary exposure to low doses of EDCs might not induce any adverse effects on the female genital system in mammals including humans. (J Toxicol Pathol 2004; 17: 69-83)

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The influence of gonadectomy, androgen exposure, or a gonadal graft in the neonatal rat on the volume of the sexually dimorphic nucleus of the preoptic area

Cited by 196 publications

References 14 publications

Developmental programming and endocrine disruptor effects on reproductive neuroendocrine systems

Developmental programming and endocrine disruptor effects on reproductive neuroendocrine systems

Quantitative estimation of estrogen and androgen receptor-immunoreactive cells in the forebrain of neonatally estrogen-deprived male rats

Toxicologic/carcinogenic Effects of Endocrine Disrupting Chemicals on the Female Genital Organs of Rodents

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