scholarly journals Unaltered Development of the Initial Follicular Waves and Normal Pubertal Onset in Female Rats after Neonatal Deletion of the Follicular Reserve

Endocrinology ◽  
2003 ◽  
Vol 144 (8) ◽  
pp. 3651-3662 ◽  
Author(s):  
Céline J. Guigon ◽  
Séverine Mazaud ◽  
Maguelone G. Forest ◽  
Sylvie Brailly-Tabard ◽  
Noëlline Coudouel ◽  
...  
2016 ◽  
Vol 35 (12) ◽  
pp. 1276-1285 ◽  
Author(s):  
R Yang ◽  
Y-M Wang ◽  
L Zhang ◽  
Z-M Zhao ◽  
J Zhao ◽  
...  

T-2 toxin, a naturally produced Type A trichothecene mycotoxin, has been shown to damage the reproductive and developmental functions in livestocks. However, whether T-2 toxin can disturb the pubertal onset and development following prepubertal exposure remains unclear. To clarify this point, infantile female Sprague–Dawley rats were given a daily intragastric administration of vehicle or T-2 toxin at a dose of 375 μg/kg body weight for 5 consecutive days from postnatal day (PND) 15–19 (PND15–PND19). The days of vaginal opening, first diestrus, and first estrus in regular estrous cycle were advanced following T-2 toxin treatment, indicating prepubertal exposure to T-2 toxin induced the advancement of puberty onset. The relative weights of uterus and ovaries and the incidence of corpora lutea were all increased in T-2 toxin-treated rats; serum hormone levels of luteinizing hormone and estradiol and the messenger RNA expressions of gonadotropin-releasing hormone (GnRH) and GnRH receptor also displayed marked increases following exposure to T-2 toxin, all of which were well consistent with the manifestations of the advanced puberty onset. In conclusion, the present study reveals that prepubertal exposure to a high level of T-2 toxin promotes puberty onset in infantile female rats by advancing the initiation of hypothalamic–pituitary–gonadal axis function in female rats.


2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Oytun Erbaş ◽  
Levent Akman ◽  
Altuğ Yavaşoğlu ◽  
Mustafa Cosan Terek ◽  
Tülay Akman ◽  
...  

Cisplatin (CP), an antitumor agent, has been shown to cause ovarian injury and dysfunction in both animal and human studies. The present study was conducted to investigate the protective effect of oxytocin (OT) on CP-induced ovarian toxicity in rats. Twenty-one adult female rats were included in the study. Fourteen rats were administered intraperitoneally CP (2 mg/kg/day) twice a week for 5 weeks. Control group (n=7) did not receive any treatment. Following treatment, CP-received rats were randomly divided into two groups and treated with either saline (1 mL/kg/day,n=7) or OT (160 μg/kg/day,n=7) for 5 weeks. Then, ovarian toxicity and effects of OT were evaluated by histomorphological and biochemical analysis. Our findings revealed a significant reduction in the number of follicles at each grade in saline-treated group. AMH level was significantly lower in saline group compared to control (P<0.0005). OT treatment significantly attenuated CP toxicity in ovaries and increased AMH levels compared to saline group (P<0.005). Also, administration of OT lessened lipid peroxidation and prevented glutathione depletion in CP-treated rats (P<0.05). These results indicated that OT could lessen the CP-induced ovarian damage and improve follicular reserve by preventing oxidative damage.


2021 ◽  
Author(s):  
Esra Kutlu ◽  
İlker Tolga Özgen ◽  
Huri Bulut ◽  
Abdurrahim Koçyiğit ◽  
Savaş Üstünova ◽  
...  
Keyword(s):  

2021 ◽  
Author(s):  
Azure Dominique Grant ◽  
Linda Wilbrecht ◽  
Lance J Kriegsfeld

Biological rhythms in core body temperature (CBT) provide informative markers of adolescent development under controlled laboratory conditions. However, it is unknown if these markers are preserved under more variable naturalistic conditions, and if CBT may therefore prove useful in a real-world setting. To evaluate this possibility, we examined fecal steroid concentrations and CBT rhythms from pre-adolescence (p26) through early adulthood (p76) in intact male and female rats under natural light and climate at the University of California, Berkeley Field Station. Despite greater environmental variability, CBT markers of pubertal onset and its rhythmic progression were comparable to those previously reported in laboratory conditions in female rats and extend actigraphy-based findings in males. Specifically, sex differences emerged in circadian rhythm (CR) power and temperature amplitude prior to pubertal onset and persisted into early adulthood, with females exhibiting elevated CBT and decreased CR power compared to males. Within-day (ultradian rhythm; UR) patterns also exhibited a pronounced sex difference associated with estrous cyclicity. Pubertal onset, defined by vaginal opening, preputial separation, and sex steroid concentrations, occurred later than previously reported under lab conditions for both sexes. Vaginal opening and increased fecal estradiol concentrations were closely tied to the commencement of 4-day oscillations in CBT and UR power in female rats. By contrast, preputial separation and the first rise in testosterone concentration were not associated with adolescent changes to CBT rhythms in male rats. Together, males and females exhibited unique temporal patterning of CBT and sex steroids across pubertal development, with tractable associations between hormonal concentrations, external development, and temporal structure in females. The preservation of these features outside the laboratory supports CBT as a strong candidate for translational pubertal monitoring under naturalistic conditions in females.


2021 ◽  
Author(s):  
Carly M. Drzewiecki ◽  
Elli P. Sellinger ◽  
Janice M. Juraska

AbstractIn female rats, pubertal onset is associated with maturation of the medial prefrontal cortex (mPFC) and mPFC-mediated behaviors. These behavioral and anatomical changes are likely due to effects of estrogen at the nuclear estrogen receptor beta (ERβ), which is expressed at higher levels than the estrogen receptor alpha (ERα) isoform in the adult mPFC. Researchers have previously quantified ERβ protein and Esr2 RNA in rodents during early postnatal development and adulthood, but an adolescent-specific trajectory of this receptor in the mPFC has not been documented. Given that levels of Esr2 can fluctuate in the presence or absence of estrogens, puberty and the subsequent rise in gonadal hormones could influence ERβ expression in the adolescent brain. To further explore this, we used RNAscope to quantify the amount of Esr2 mRNA in pre-pubertal adolescent, recently post-pubertal adolescent, and adult female rats. We show here that Esr2 expression decreases significantly in the mPFC, striatum and motor cortex between pre-pubertal adolescence and adulthood. In the mPFC, this decrease occurs rapidly at pubertal onset, with no significant decrease in Esr2 levels between the recently post-pubertal and adult cohort. In contrast in the striatum and motor cortex, there were no significant differences in the amount of Esr2 between pre- and post-pubertal females. Insofar as the amount of Esr2 is proportional to functional ERβ, these results suggest ERβ decreases in a region-specific pattern in response to pubertal onset and highlight a role for this receptor in the maturational events that occur in the female rat mPFC at puberty.


2021 ◽  
Author(s):  
Yoo-Mi Kim ◽  
Han H. Lim

Abstract Background Central precocious puberty is caused by early activation of the hypothalamic–pituitary–gonadal axis but its major cause remains unclear. Studies have indicated an association between chronic environmental exposure to endocrine-disrupting chemicals and pubertal onset. Methods To evaluate this association, we compared the hormone levels and timing of vaginal opening in female rats exposed to lavender oil (LO) through different routes [study groups: control, LO nasal spray (LS), and indoor exposure to LO (LE)] during the prepubertal period. The body weights of the animals were also compared every 3 days until the day of vaginal opening, at which time gonadotropin levels and internal organ weights were assessed. Results The LS group showed early vaginal opening at 33.8 ± 1.8 days compared with the control (38.4 ± 2.9 days) and LE (36.6 ± 1.5 days) groups. Additionally, luteinizing hormone levels were significantly higher in the LE and LS groups than in the control group. Body weights did not differ significantly among the groups. Conclusions Exposure to an exogenic simulant via inhalation during the prepubertal period triggered early puberty onset in female rats. Further evaluation of exposure to other endocrine-disrupting chemicals capable of inducing central precocious puberty through the skin, orally, and/or nasally is warranted.


Author(s):  
Carly M. Drzewiecki ◽  
Jari Willing ◽  
Janice M. Juraska

AbstractThe prefrontal cortex (PFC) is a late developing region of the cortex, and its protracted maturation during adolescence may confer a period of plasticity. Closure of critical, or sensitive, periods in sensory cortices coincides with perineuronal net (PNN) expression, leading to enhanced inhibitory function and synaptic stabilization. PNN density is known to increase across adolescence in the male rodent medial PFC (mPFC). However, the trajectory of female PNN development has not been explored nor has the potential role of pubertal onset in PNN expression. Here, we examined rats at four time points spanning adolescent development to quantify the number of PNNs in the mPFC, as well as the total volume of the prefrontal white matter. Additionally, because puberty coincides with broad behavioral and neuroanatomical changes, we collected tissue from age-matched pre- and post- pubertal siblings within a litter. Results indicate that both males and females show an increase the total number of mPFC PNNs and in white matter under the mPFC between postnatal day (P) 30 and P60. Male puberty did not affect PNNs, while female pubertal onset led to an abrupt decrease in the total number of PNNs that persisted through mid-adolescence before increasing at P60. This decrease in female rats may indicate a difference in timing of maximal plasticity between the sexes during adolescence.


Author(s):  
I. Russo ◽  
J. Saby ◽  
J. Russo

It has been previously demonstrated that DMBA-induced rat mammary carcinoma originates in the terminal end bud (TEB) of the mammary gland by proliferation of intermediate type cells (1). The earliest lesion identified is the intraductal proliferation (IDP), which gives rise to intraductal carcinomas. These evolve to cribriform, papillary and comedo types (2). In the present work, we report the ultrastructural changes that take place in the IDP for the formation of a cribriform pattern.Fifty-five-day-old Sprague Dawley virgin female rats were inoculated intra- gastrically with 20 mg 7,12-dimethylbenz(a)anthracene (DMBA) in 1 ml sesame oil. Non-inoculated, age-matched females were used as controls. Mammary glands from both control and experimental rats were removed weekly from the time of inoculation until 86 days post-inoculation. The glands were fixed and processed for electron microscopy (2).The first change observed in IDP's was the widening of intercellular spaces and the secretion of an electron dense material into these spaces (Fig. 1).


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