Neonatal exposure to technical methoxychlor alters pregnancy outcome in female mice

Abstract Background: In animal models, exposure to general anesthetics induces widespread increases in neuronal apoptosis in the developing brain. Subsequently, abnormalities in brain functioning are found in adulthood, long after the anesthetic exposure. These abnormalities include not only reduced learning abilities but also impaired social behaviors, suggesting pervasive deficits in brain functioning. But the underlying features of these deficits are still largely unknown. Methods: Six-day-old C57BL/6 female mice were exposed to 3% sevoflurane for 6 h with or without hydrogen (1.3%) as part of the carrier gas mixture. At 7–9 weeks of age, they were mated with healthy males. The first day after parturition, the maternal behaviors of dams were evaluated. The survival rate of newborn pups was recorded for 6 days after birth. Results: Female mice that received neonatal exposure to sevoflurane could mate normally and deliver healthy pups similar to controls. But these dams often left the pups scattered in the cage and nurtured them very little, so that about half of the pups died within a couple of days. Yet, these dams did not show any deficits in olfactory or exploratory behaviors. Notably, pups born to sevoflurane-treated dams were successfully fostered when nursed by control dams. Mice coadministered of hydrogen gas with sevoflurane did not exhibit the deficits of maternal behaviors. Conclusion: In an animal model, sevoflurane exposure in the developing brain caused serious impairment of maternal behaviors when fostering their pups, suggesting pervasive impairment of brain functions including innate behavior essential to species survival.

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Neonatal exposure to sevoflurane impairs preference for social novelty in C57BL/6 female mice at early-adulthood

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2022.01.022 ◽

2022 ◽

Author(s):

Huayue Liu ◽

Xiaowen Meng ◽

Yixuan Li ◽

Shiwen Chen ◽

Yumen Ji ◽

...

Keyword(s):

Early Adulthood ◽

Neonatal Exposure ◽

Female Mice

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Mouse anococcygeus muscle: sexual dimorphism and responsiveness to sex hormones

Journal of Endocrinology ◽

10.1677/joe.0.1520229 ◽

1997 ◽

Vol 152 (2) ◽

pp. 229-237 ◽

Cited By ~ 7

Author(s):

Y Fukazawa ◽

T Iguchi ◽

H A Bern

Keyword(s):

Sexual Dimorphism ◽

Oestrogen Receptor ◽

Strain Differences ◽

Neonatal Exposure ◽

Thin Sheets ◽

Male Mice ◽

Cross Sectional ◽

Female Mice ◽

Anococcygeus Muscle ◽

Icr Mice

Abstract The anococcygeus muscle (AcM) is one of a pair of thin sheets of smooth muscle inserting on the rectum, having a tendinous origin largely on sacral vertebrae. The cross-sectional area of AcM in the juxtarectal region in 90-day-old male mice was significantly larger than that in females of three strains: BALB/cCrgl, ICR/Jcl and C57BL/Tw. The AcM area in female mice showed strain differences: BALB/c>ICR>C57BL. Five daily injections of testosterone into newborn ICR mice from the day of birth significantly increased the areas of AcM in both sexes at 30 days of age, but five daily injections of oestradiol-17β (OE) decreased them. The AcM area in 60-day-old ICR male mice castrated at 30 days of age was significantly smaller than in intact males, and that in ovariectomized females was significantly larger than in intact females. In both sexes, implantation of a testosterone pellet (12 mg) into gonadectomized mice on the day of gonadectomy stimulated the growth of AcM, and implantation of an OE pellet (12 mg) inhibited the growth of AcM. The AcM in both ICR and C57BL strains showed positive androgen receptor and oestrogen receptor immunostaining at 15 days. Female ICR mice exposed neonatally to diethylstilboestrol (DES) had significantly larger AcM than controls; ovariectomy at 30 days of age did not change the AcM area in 60-day-old DES-exposed mice. However, male mice exposed neonatally to DES had significantly smaller AcM than controls; castration at 30 days of age nullified this inhibition. These results suggest that both androgen and oestrogen play an important role in sexual dimorphism of the mouse AcM. Neonatal exposure to DES (but not to oestradiol) had an irreversible stimulatory effect on the AcM area in female mice. Journal of Endocrinology (1997) 152, 229–237

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Evaluation of Neonatal Exposure to Mycoestrogens Zearalenone and Alpha-zearalenol on Puberty and Reproductive Function in Female Mice

journal of ilam university of medical sciences ◽

10.18869/acadpub.sjimu.24.6.11 ◽

2017 ◽

Vol 24 (6) ◽

pp. 11-22

Author(s):

Rahmatollah Parandin ◽

Morteza Behnam Rassouli ◽

Nasser Mahdavi Shahri ◽

◽

...

Keyword(s):

Reproductive Function ◽

Neonatal Exposure ◽

Female Mice

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Normal ovarian aging, but modified T-cell differentiation, in female mice following neonatal exposure to bisphenol A

Fundamental Toxicological Sciences ◽

10.2131/fts.4.15 ◽

2017 ◽

Vol 4 (1) ◽

pp. 15-21

Author(s):

Ryo Ohta ◽

Hideo Ohmukai ◽

Tsukasa Negura ◽

Yoshiyuki Tazura ◽

Tomoko Shindo

Keyword(s):

Cell Differentiation ◽

T Cell ◽

Bisphenol A ◽

T Cell Differentiation ◽

Neonatal Exposure ◽

Female Mice ◽

Ovarian Aging

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In vitro exposure of male and female mice gametes to cadmium chloride during the fertilization process, and its effects on pregnancy outcome

Toxicology and Applied Pharmacology ◽

10.1016/0041-008x(83)90256-9 ◽

1983 ◽

Vol 69 (3) ◽

pp. 326-332 ◽

Cited By ~ 19

Author(s):

B.P. Schmid ◽

J.L. Hall ◽

E. Goulding ◽

S. Fabro ◽

R. Dixon

Keyword(s):

Pregnancy Outcome ◽

Cadmium Chloride ◽

Male And Female ◽

Fertilization Process ◽

Female Mice ◽

In Vitro Exposure

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Early-Life Exposure to Testosterone Programs the Hypothalamic Melanocortin System

Endocrinology ◽

10.1210/en.2010-1288 ◽

2011 ◽

Vol 152 (4) ◽

pp. 1661-1669 ◽

Cited By ~ 78

Author(s):

Kazunari Nohara ◽

Yan Zhang ◽

Rizwana S. Waraich ◽

Amanda Laque ◽

Joseph P. Tiano ◽

...

Keyword(s):

Food Intake ◽

Energy Intake ◽

Underlying Mechanism ◽

Leptin Resistance ◽

Neonatal Exposure ◽

Dependent Manner ◽

Melanocortin System ◽

Female Mice ◽

Early Life Exposure ◽

Hypothalamic Arcuate Nucleus

Abstract In mammals, males consume more food, which is considered a masculinized behavior, but the underlying mechanism of this sex-specific feeding behavior is unknown. In mice, neonatal testosterone (NT) is critical to masculinize the developing brain, leading to sex differences in reproductive physiology. The proopiomelanocortin (POMC) neurons of the hypothalamic arcuate nucleus (ARC) are critical to suppress energy intake and POMC innervation of hypothalamic feeding circuits develops to a large extent neonatally. We hypothesized that NT programs the masculinization of energy intake by programming POMC neurons. We tested this hypothesis by comparing control females and control males (CMs) with female mice neonatally androgenized with testosterone (NTFs). We show that increased food intake in CMs is associated with reduced POMC expression and decreased intensity of neuronal projections from POMC neurons within the ARC compared with control females. We found that NTFs display a masculinized energy intake and ARC POMC expression and innervation as observed in CMs, which can be mimicked by neonatal exposure to the androgen receptor agonist dihydrotestosterone (DHT). NTFs also exhibit hyperleptinemia and a decreased ability of leptin to up-regulate POMC, suppress food intake, and prevent adipose tissue accumulation, independent of signal transducer and activator of transcription 3. However, this leptin resistance is specific to NTFs, is not a consequence of masculinization, and is reproduced by neonatal exposure to estrogen but not DHT. Thus, NT programs a sexual differentiation of POMC neurons in female mice via DHT but also predisposes to leptin resistance and obesity in an estrogen-dependent manner.

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