scholarly journals Type 1 5α-reductase may be required for estrous cycle changes in affective behaviors of female mice

2012 ◽  
Vol 226 (2) ◽  
pp. 376-380 ◽  
Author(s):  
Carolyn J. Koonce ◽  
Alicia A. Walf ◽  
Cheryl A. Frye
1983 ◽  
Vol 17 (2) ◽  
pp. 233-236 ◽  
Author(s):  
A. Marchlewska-Koj ◽  
M. Kruczek ◽  
E. Toch
Keyword(s):  

2014 ◽  
Vol 229 ◽  
pp. S237
Author(s):  
Claudio Filgueiras ◽  
Ulisses Araujo ◽  
Fernanda Nunes ◽  
Bruno Gonçalves ◽  
Regina Gomes ◽  
...  

2007 ◽  
Vol 193 (1) ◽  
pp. 127-135 ◽  
Author(s):  
Hwa-Yong Lee ◽  
Tomas J Acosta ◽  
Michiyo Tanikawa ◽  
Ryosuke Sakumoto ◽  
Junichi Komiyama ◽  
...  

To determine whether glucocorticoids (GCs) play a role in regulating uterine function in cow, the present study examined the expression of mRNA encoding GC receptor (GC-R) α, 11β-hydroxysteroid dehydrogenase (11-HSD) type 1 and type 2, and the activity of 11-HSD1 in bovine endometrial tissue throughout the estrous cycle. We also studied the effects of cortisol on basal, oxytocin (OT)- and tumor necrosis factor-α (TNFα)-stimulated prostaglandin (PG) production. A quantitative real-time PCR analysis revealed that GC-Rα mRNA was expressed more strongly in the mid-luteal stage (days 8–12) than in the other stages. In contrast to GC-Rα mRNA expression, 11-HSD1 mRNA expression was greater in the follicular stage than in the other stages, whereas 11-HSD2 mRNA expression was lowest in the follicular stage. The activity of 11-HSD1 was greater in the follicular stage and estrus than in the other stages and was lowest in the mid-luteal stage. Cortisone was dose-dependently converted to cortisol in the cultured endometrial tissue. Although cortisol did not affect either the basal or OT-stimulated production of PGs in the cultured epithelial cells, the production of PGs stimulated by TNFα in the stromal cells was suppressed by cortisol (P < 0.05). Cortisol suppressed basal prostaglandin (PG)F2α without affecting basal PGE2 production in the stromal cells. The overall results suggest that the level of cortisol is locally regulated in bovine endometrium throughout the estrous cycle by 11-HSD1, and that cortisol could act as a luteoprotective factor by selectively suppressing luteolytic PGF2α production in bovine endometrium.


2015 ◽  
Vol 117 (3) ◽  
pp. 297-304 ◽  
Author(s):  
Yalei Wang ◽  
Chenling Meng ◽  
Quanwei Wei ◽  
Fangxiong Shi ◽  
Dagan Mao

2014 ◽  
Vol 306 (7) ◽  
pp. H938-H953 ◽  
Author(s):  
Jennifer K. MacDonald ◽  
W. Glen Pyle ◽  
Cristine J. Reitz ◽  
Susan E. Howlett

This study established conditions to induce regular estrous cycles in female C57BL/6J mice and investigated the impact of the estrous cycle on contractions, Ca2+ transients, and underlying cardiac excitation-contraction (EC)-coupling mechanisms. Daily vaginal smears from group-housed virgin female mice were stained to distinguish estrous stage (proestrus, estrus, metestrus, diestrus). Ventricular myocytes were isolated from anesthetized mice. Contractions and Ca2+ transients were measured simultaneously (4 Hz, 37°C). Interestingly, mice did not exhibit regular cycles unless they were exposed to male pheromones in bedding added to their cages. Field-stimulated myocytes from mice in estrus had larger contractions (∼2-fold increase), larger Ca2+ transients (∼1.11-fold increase), and longer action potentials (>2-fold increase) compared with other stages. Larger contractions and Ca2+ transients were not observed in estrus myocytes voltage-clamped with shorter action potentials. Voltage-clamp experiments also demonstrated that estrous stage had no effect on Ca2+ current, EC-coupling gain, diastolic Ca2+, sarcoplasmic reticulum (SR) Ca2+ content, or fractional release. Although contractions were largest in estrus, myofilament Ca2+ sensitivity was lowest (EC50 values ∼1.15-fold higher) in conjunction with increased phosphorylation of myosin binding protein C in estrus. Contractions were enhanced in ventricular myocytes from mice in estrus because action potential prolongation increased SR Ca2+ release. These findings demonstrate that cyclical changes in reproductive hormones associated with the estrous cycle can influence myocardial electrical and contractile function and modify Ca2+ homeostasis. However, such changes are unlikely to occur in female mice housed in groups under conventional conditions, since these mice do not exhibit regular estrous cycles.


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