scholarly journals Somatostatin in the Periventricular Nucleus of the Female Rat: Age Specific Effects of Estrogen and Onset of Reproductive Aging

Sex Steroids ◽  
10.5772/27872 ◽  
2012 ◽  
Author(s):  
Eline M. Van der Beek ◽  
Harmke H. Van Vugt ◽  
Annelieke N. ◽  
Bert J.M. Van de Heijning

1990 ◽  
Vol 52 (5) ◽  
pp. 527-536 ◽  
Author(s):  
Ricardo Zorrilla ◽  
Jacques Simard ◽  
Eric Rhéaume ◽  
Fernand Labrie ◽  
Georges Pelletier


2016 ◽  
Vol 61 ◽  
pp. 186-194 ◽  
Author(s):  
Hanna Katarina Lilith Johansson ◽  
Pernille Rosenskjold Jacobsen ◽  
Ulla Hass ◽  
Terje Svingen ◽  
Anne Marie Vinggaard ◽  
...  




Endocrine ◽  
1995 ◽  
Vol 3 (5) ◽  
pp. 327-333 ◽  
Author(s):  
Ming H. Jih ◽  
Tsung-Chieh J. Wu


Endocrinology ◽  
2008 ◽  
Vol 150 (1) ◽  
pp. 376-384 ◽  
Author(s):  
Jill K. Hiney ◽  
Vinod K. Srivastava ◽  
Michelle D. Pine ◽  
W. Les Dees

KiSS-1 gene expression has been shown to increase as puberty approaches, and its peptide products, kisspeptins, are involved in LHRH secretion at puberty. Factors contributing to increased KiSS-1 expression, however, have not been identified; thus, the purpose of this study was to assess whether IGF-I could induce transcription of this gene in prepubertal female rats. IGF-I or saline was centrally administered to immature rats that were killed 2, 4, and 6 h later. Real-time PCR revealed that IGF-I induced (P < 0.01) KiSS-1 gene expression at 6 h in a tissue fragment that contained both the anteroventral periventricular (AVPV) and arcuate (ARC) nuclei. Subsequently, the AVPV and ARC nuclei were separated to assess whether region-specific effects could be identified. IGF-I stimulated (P < 0.01) KiSS-1 gene expression in the AVPV nucleus at 6 h after injection, with no change observed in the ARC nucleus. Serum estradiol (E2) levels were not altered at any time point after IGF-I, demonstrating that the increased KiSS-1 expression observed was not caused by an elevation in E2. Additionally, the IGF-I action to induce KiSS-1 gene expression in the AVPV nucleus was further demonstrated when the IGF-I was administered systemically. E2 appears to play an important permissive role because 1-d ovariectomized rats responded to IGF-I with increased (P < 0.01) KiSS-1 expression, whereas, 20 d after ovariectomy, when the E2 levels had fallen below assay sensitivity, the IGF-I was unable to induce KiSS-1 expression. The IGF-I effect was further demonstrated by showing that the IGF-I receptor antagonist, JB-1, blocked the IGF-I-induced increase in KiSS-1 expression. Collectively, these data indicate that IGF-I is an activator of the KiSS-1 gene in the prepubertal female rat. IGF-1 is an early activator of the KiSS-1 gene at the time of female puberty.



2017 ◽  
Vol 312 (3) ◽  
pp. L405-L414 ◽  
Author(s):  
Melanie Haase ◽  
Mandy Laube ◽  
Ulrich H. Thome

Alveolar fluid clearance mediates perinatal lung transition to air breathing in newborn infants, which is accomplished by epithelial Na+ channels (ENaC) and Na-K-ATPase. Male sex represents a major risk factor for developing respiratory distress, especially in preterm infants. We previously showed that male sex is associated with reduced epithelial Na+ transport, possibly contributing to the sexual dimorphism in newborn respiratory distress. This study aimed to determine sex-specific effects of sex steroids on epithelial Na+ transport. The effects of testosterone, 5α-dihydrotestosterone (DHT), estradiol, and progesterone on Na+ transport and Na+ channel expression were determined in fetal distal lung epithelial (FDLE) cells of male and female rat fetuses by Ussing chamber and mRNA expression analyses. DHT showed a minor effect only in male FDLE cells by decreasing epithelial Na+ transport. However, flutamide, an androgen receptor antagonist, did not abolish the gender imbalance, and testosterone lacked any effect on Na+ transport in male and female FDLE cells. In contrast, estradiol and progesterone increased Na+ transport and Na+ channel expression especially in females, and prevented the inhibiting effect of DHT in males. Estrogen receptor inhibition decreased Na+ channel expression and eliminated the sex differences. In conclusion, female sex steroids stimulate Na+ transport especially in females and prevent the inhibitory effect of DHT in males. The ineffectiveness of testosterone suggests that Na+ transport is largely unaffected by androgens. Thus, the higher responsiveness of female cells to female sex steroids explains the higher Na+ transport activity, possibly leading to a functional advantage in females.





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