scholarly journals Neuroendocrine correlates of sex-role reversal in barred buttonquails

2016 ◽  
Vol 283 (1843) ◽  
pp. 20161969 ◽  
Author(s):  
Cornelia Voigt

Sex differences in brain structure and behaviour are well documented among vertebrates. An excellent model exploring the neural mechanisms of sex differences in behaviour is represented by sex-role-reversed species. In the majority of bird species, males compete over access to mates and resources more strongly than do females. It is thought that the responsible brain regions are therefore more developed in males than in females. Because these behaviours and brain regions are activated by androgens, males usually have increased testosterone levels during breeding. Therefore, in species with sex-role reversal, certain areas of the female brain should be more developed or steroid hormone profiles should be sexually reversed. Here, I studied circulating hormone levels and gene expression of steroid hormone receptors and aromatase in a captive population of barred buttonquails ( Turnix suscitator ). While females performed courtship and agonistic behaviours, there was no evidence for sexually reversed hormone profiles. However, I found female-biased sex differences in gene expression of androgen receptors in several hypothalamic and limbic brain regions that were already in place at hatching. Such sex differences are not known from non-sex-role-reversed species. These data suggest that increased neural sensitivity to androgens could be involved in the mechanisms mediating sex-role-reversed behaviours.

1994 ◽  
Vol 28 (4) ◽  
pp. 464-476 ◽  
Author(s):  
Robert J. Handa ◽  
Loyd H. Burgess ◽  
Janice E. Kerr ◽  
Joan A. O'Keefe

2007 ◽  
Vol 38 (5) ◽  
pp. 569-585 ◽  
Author(s):  
Li Li ◽  
Melvin E Andersen ◽  
Steffen Heber ◽  
Qiang Zhang

Steroid hormone receptors are the targets of many environmental endocrine active chemicals (EACs) and synthetic drugs used in hormone therapy. While most of these chemical compounds have a unidirectional and monotonic effect, certain EACs can display non-monotonic dose–response behaviors and some synthetic drugs are selective endocrine modulators. Mechanisms underlying these complex endocrine behaviors have not been fully understood. By formulating an ordinary differential equation-based computational model, we investigated in this study the steady-state dose–response behavior of exogenous steroid ligands in an endogenous hormonal background under various parameter conditions. Our simulation revealed that non-monotonic dose–responses in gene expression can arise within the classical genomic framework of steroid signaling. Specifically, when the exogenous ligand is an agonist, a U-shaped dose–response appears as a result of the inherently nonlinear process of receptor homodimerization. This U-shaped dose–response curve can be further modulated by mixed-ligand heterodimers formed between endogenous ligand-bound and exogenous ligand-bound receptor monomers. When the heterodimer is transcriptionally inactive or repressive, the magnitude of U-shape increases; conversely, when the heterodimer is transcriptionally active, the magnitude of U-shape decreases. Additionally, we found that an inverted U-shaped dose–response can arise when the heterodimer is a strong transcription activator regardless of whether the exogenous ligand is an agonist or antagonist. Our work provides a novel mechanism for non-monotonic, particularly U-shaped, dose–response behaviors observed with certain steroid mimics, and may help not only understand how selective steroid receptor modulators work but also improve risk assessment for EACs.


1992 ◽  
Vol 25 (6) ◽  
pp. 667-680 ◽  
Author(s):  
JUNZO KATO ◽  
SHUJI HIRATA ◽  
KAZUKI HAGIHARA ◽  
TAKAAKI OSADA ◽  
MITSUO HIRAI ◽  
...  

2011 ◽  
Vol 5 ◽  
pp. BCBCR.S7707 ◽  
Author(s):  
R. Jahanban Esfahlan ◽  
N. Zarghami ◽  
A. Jahanban Esfahlan ◽  
M. Mollazadeh ◽  
K. Nejati ◽  
...  

Background Obesity has been associated with increased mortality from hormone dependant cancers such as breast cancer which is the most prevalent cancer in women. The link between obesity and breast cancer can be attributed to excess estrogen produced through aromatization in adipose tissue. The role of steroid hormone receptors in breast cancer development is well studied but how obesity can affect the expression pattern of steroid hormones in patients with different grades of breast cancer was the aim of this study. Methods In this case-control study, 70 women with breast cancer participated with different grades of obesity (36 none obese, BMI < 25 kg/m2 and 34 obese, BMI ≥ 25 kg/m2). The mean age of participants was 44.53 ± 1.79 yr (21–70 yr). The serum level of estrogen, progesterone and androgen determined by ELISA. Following quantitative expression of steroid hormone receptors mRNA in tumor tissues evaluated by Real-time PCR. Patients with previous history of radiotherapy or chemotherapy were excluded. SPSS 16 was used for data analysis and P < 0.05 considered statistically significant. Results The difference in ERα, ERβ and PR mRNA level between normal and obese patients was significant ( P < 0.001). In addition, the expression of AR mRNA was found to be higher than other steroid receptors. There was no significant relation between ERβ gene expression in two groups ( P = 0.68). We observed a significant relationship between ERα and AR mRNA with tumor stage and tumor grade, respectively ( P = 0.023, P = 0.015). Conclusion According to the obtained results, it is speculated that obesity could paly a significant role in estrogen receptors gene expression and also could affect progression and proliferation of breast cancer cells.


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