Vaginal opening and vaginal epithelium following ovariectomy in newborn rats

Gitlin, Gershon

doi:10.1159/000144329

Cited by 3 publications

(4 citation statements)

References 8 publications

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“…We have chosen this age because it corresponds to the time‐point in which the ovaries become capable of secreting significant amounts of their hormones (Lamprecht et al, 1976). In accordance with a previous report (Gitlin, 1974), the effectiveness of the ovariectomy was presently evidenced by the severe atrophic patterns of uterus‐ and genital‐epithelium, delayed vaginal opening, and body weight increment, as compared to the controls. Regarding the ovariectomy‐induced increase in body weights, it is known that the hypoestrogenic status participates in the increased food intake and the resulting higher body weight gain, as compared to the controls (Wade, 1975; Roesch, 2006).…”

Section: Discussionsupporting

confidence: 91%

Ovariectomy in the developing rat decelerates cortical spreading depression in adult brain

Accioly

Benevides²,

Costa

et al. 2012

Intl J of Devlp Neuroscience

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The brain of mammals is one important target organ for the action of gonadal steroids and, when occurring during development, this hormonal influence may result in important repercussion on the brain electrophysiological properties at adulthood, some of which depending on the brain excitability. Here we have characterized in early-ovariectomized adult rats the brain ability to propagate the excitability-related phenomenon known as cortical spreading depression (CSD), as an index of the cerebral electrophysiological effects of the early-induced absence of the ovarian hormones. Wistar female rat pups (7-day old) underwent bilateral ovariectomy (Ovx group; n=21) or Sham surgery (Sham group; n=22), or no surgery (Naive group; n=22). When the pups became adult (90-130 days), they were submitted to the recording of CSD (electrocorticogram and slow DC-voltage variation) in two points of the cortical surface during 4h. Compared with both Naïve and Sham controls, bilateral ovariectomy early in life resulted in significantly higher body weights (from days 50-65 onwards) and severely reduced uterus weights at adulthood. Furthermore, in the Ovx animals the amplitudes and durations of the DC-potential changes of CSD were higher, and the CSD propagation velocities were reduced. Another group of rats ovariectomized in adulthood did not present such CSD alterations. It is concluded that ovariectomy during brain development is causally associated with the CSD changes in the adult brain, indicating a long-lasting effect, which we suggest as being related to the long-term suppression of the action of the ovarian hormones on brain excitability.

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Section: Discussionsupporting

confidence: 91%

Ovariectomy in the developing rat decelerates cortical spreading depression in adult brain

Accioly

Benevides²,

Costa

et al. 2012

Intl J of Devlp Neuroscience

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“…As shown in Figure 6, VO was advanced in the ovariectomized rats that received stanozolol as compared with the ovariectomized rats that received the oil vehicle (F(1, 14) ϭ 28.0, P Ͻ 0.05), indicating that the ovaries are not necessary for the advancement of VO by stanozolol. As of PN60, in agreement with previous published studies [18,19], a portion of the ovariectomized/oil rats exhibited VO (five of eight rats). The three rats that did not exhibit VO during the experiment were assigned a value of PN60 in the analysis.…”

Section: Acute Effects Of Stanozolol Treatment On Aspects Of Pubertalsupporting

confidence: 91%

Effects of Acute Stanozolol Treatment on Puberty in Female Rats1

Whitney¹,

Clark²

2001

Biology of Reproduction

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The effects of anabolic-androgenic steroid (AAS) abuse on the onset of puberty in female adolescents are largely unknown. This study assessed the acute effects of one AAS, stanozolol, on pubertal onset in the female rat. A single injection of stanozolol (5 mg/kg) on Postnatal Day (PN) 21 advanced vaginal opening but did not alter the onset of vaginal estrus. Higher doses of stanozolol treatment (10 and 25 mg/kg) also advanced vaginal opening but had no effect on vaginal estrus. The advancement of vaginal opening by stanozolol (5 mg/kg) was prevented by the concomitant administration of the pure antiestrogen ICI 182,780 (1 mg/kg) on PN20-22. Administration of the androgen receptor antagonist flutamide (10 mg/kg twice daily) on PN20-22 had no effect on the advancement of vaginal opening by stanozolol. Stanozolol treatment also advanced vaginal opening in ovariectomized rats. Perivaginal injections of a low dose of stanozolol (0.05 mg) on PN21 and PN23 also advanced vaginal opening. These results suggest that stanozolol is acting directly at estrogen receptors in the vaginal epithelium to advance vaginal opening and that prepubertal stanozolol treatment does not induce true precocious puberty.

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“…Vaginal opening is a clear-cut, easily measurable example of an estrogen-dependent event critical to the development of the reproductive system. At birth, the rodent vaginal canal is closed to the outside environment by stratified epithelial cells (Gitlin, 1974). During development, the vagina in the rodent responds to rising endogenous estrogen levels at puberty and the solid cells of the vaginal canal are deleted, resulting in an opening (Elger, 1978;Ojeda et al, 1980).…”

Section: Effects Of Estrogenic Endocrine Disrupting Chemicalsmentioning

confidence: 99%

“…The molecular mechanism by which estrogen induces vaginal opening in the rodent is not known. Vaginal opening may occur as a result of estrogen-induced terminal cell differentiation in a target cell population leading to cell loss (Gitlin 1974), or vaginal opening may result from programmed cell death that causes a deletion of specific epithelial cells that form the vaginal plate (Gray Jr. & Ostby, 1995).…”

Section: Effects Of Estrogenic Endocrine Disrupting Chemicalsmentioning

confidence: 99%