Intracerebral Infusion of an Aromatase Inhibitor, Sexual Behavior and Brain Estrogen Receptor-Like Immunoreactivity in Intact Male Rats

1995 ◽  
Vol 61 (2) ◽  
pp. 98-111 ◽  
Author(s):  
Andrew N. Clancy ◽  
Doris Zumpe ◽  
Richard P. Michael
2019 ◽  
Vol 43 (4) ◽  
pp. 458-466
Author(s):  
Rodney D. Geisert ◽  
Amanda L. Schmelzle ◽  
Michael F. Smith ◽  
Jonathan A. Green

In this teaching laboratory, students design and perform an experiment to determine estrogen’s role in imprinting the brain of neonatal rats to express either male or female sexual behavior. A discussion question is provided before the laboratory exercise in which each student is asked to search the literature and provide written answers to questions and to formulate an experiment to test the role of estrogen in imprinting the mating behavior of male and female rats. Students discuss their answers to the questions in laboratory with the instructor and design an experiment to test their hypothesis. In male rats, testosterone is converted by aromatase expressed by neurons in the brain to estrogen. Production of estrogen in the brain of neonatal rats imprints mating behavior in males, where a lack of estrogen action in the brain imprints female sexual behavior. The model involves administering exogenous testosterone to imprint male behavior in female pups or administration of an aromatase inhibitor (letrozole) or an estrogen receptor antagonist (ICI 182,780) to imprint female sexual behavior in male pups. In the model, litters of neonatal pups are treated with either carrier (control), testosterone propionate, aromatase inhibitor (letrozole), or an estrogen receptor antagonist (ICI 182,780) postnatally on days 1 and 3. Alteration of mating behavior is evaluated through the numbers of males and females that breed and establish pregnancy. This is a very simple protocol that provides an excellent experiment for student discussion on the effects of hormone action on imprinting brain sexual behavior.


2013 ◽  
Vol 305 (1) ◽  
pp. E113-E118 ◽  
Author(s):  
Sarah H. Lindsey ◽  
Ariel S. da Silva ◽  
Mauro S. Silva ◽  
Mark C. Chappell

Previously, we reported that chronic activation of the estrogen receptor GPR30 by its selective agonist G-1 decreases blood pressure in ovariectomized hypertensive mRen2.Lewis (mRen2) rats but not intact male littermates. Furthermore, G-1 relaxes female mesenteric resistance arteries via both endothelium-dependent and -independent mechanisms. Because of the lack of a blood pressure-lowering effect by G-1 in males and the potential influence of aging on estrogen receptor expression, we hypothesized that GPR30-dependent vasodilation and receptor expression are altered in males and aged females. Thus, we assessed the response to 17β-estradiol or G-1 in mesenteric arteries obtained from 15-wk-old normotensive Lewis and hypertensive mRen2 females and males as well as 52-wk-old Lewis females. Vasodilation to 17β-estradiol (E2) and G-1 was significantly attenuated in 15-wk-old Lewis and mRen2 males compared with age-matched females. Pretreatment of male vessels with the nitric oxide synthase inhibitor l-NAME had no significant effect on the estradiol or G-1 response. In aged females, E2 and G-1 vasorelaxation was also significantly blunted; however, l-NAME essentially abolished the response. Associated with the reduced vascular responses, GPR30 expression in mesenteric arteries was approximately 50% lower in males and aged females compared with young females. We conclude that alterations in GPR30 expression and signaling may contribute to vascular dysfunction in aging females and a greater blood pressure in hypertensive males.


1997 ◽  
Vol 31 (1) ◽  
pp. 35-46 ◽  
Author(s):  
Ann S. Clark ◽  
Elizabeth V. Harrold ◽  
Alison S. Fast

2020 ◽  
Vol 98 (Supplement_3) ◽  
pp. 148-149
Author(s):  
Sara K Gholson ◽  
Amanda Schmelzle ◽  
Jonathon Green ◽  
Micheal Smith ◽  
Rodney Geisert

Abstract The mammalian brain is sexually dimorphic until becoming imprinted before birth or during neonatal development. The naïve mammalian brain of neonates is programmed to become feminine. In male neonates, testosterone crosses the blood brain barrier where it is converted to estrogen by aromatase. Estrogen in the brain imprints male sexual behavior. In female neonates, estrogen binds to alpha fetoprotein which prohibits estrogen from entering the brain. The present study was undertaken to determine if testosterone, an estrogen receptor antagonist (ICI 182,780) or aromatase inhibitor (Letrozole) would alter sexual behavior in neonatal rats. In this study, the entire litter of neonatal rat pups received a sc injection (100µl) of one of the following four treatments: corn oil (CO), testosterone propionate 100 µg (TP), ICI 182,780 100 µg (ICI), or Letorozole 100 µg (LET) on days 1 and 3 after birth. At approximately 60-70 days of age, treated rats were placed in cages with nontreated rats of the opposite sex. Animals were euthanized after 20 days. Body, testis, epididymal, and accessory gland weights were recorded for males as well as the number of females they bred and litter size. Body weight, pregnancy status, and litter size (if pregnant) were recorded for treated females. While there was a difference (P< 0.001) in body weight between males and females (average 372 g vs 279 g respectively), there was no statistical differences in body, testis, epididymal, or accessory gland weight between male treatment groups. While number of females pregnant or litter size was not different for CO, TP, or ICI, LET males established no pregnancies. Body weight, number pregnant and litter size were not different between female CO, ICI, or LET treatments. However, TP treated females established no pregnancies. Sexual mating behavior is altered by neonatal exposure to an aromatase inhibitor or testosterone in rats.


1977 ◽  
Vol 91 (6) ◽  
pp. 1417-1423 ◽  
Author(s):  
Ingeborg L. Ward ◽  
JoAnn E. Franck ◽  
William R. Crowley

2004 ◽  
Vol 171 (4S) ◽  
pp. 429-429
Author(s):  
Masayoshi Nomura ◽  
Naohiro Fujimoto ◽  
Donald W. Pfaff ◽  
Sonoko Ogawa ◽  
Tetsuro Matsumoto

1981 ◽  
Vol 96 (2) ◽  
pp. 273-280 ◽  
Author(s):  
Mridula Chowdhury ◽  
Robert Tcholakian ◽  
Emil Steinberger

Abstract. It has been suggested that treatment of intact male rats with oestradiol benzoate (OeB) causes an interference with testosterone (T) production by the testes by a direct inhibitory effect on steroidogenesis. To test this hypothesis, different doses (5, 10 or 25 IU) of hCG were administered concomitantly with 50 μg of OeB to adult intact or hypophysectomized male rats. The testicular and plasma testosterone, and serum hCG levels were determined. The sex accessory weights were recorded. In the intact OeB-treated group of animals, hCG stimulated both the secondary sex organs and plasma testosterone levels above the intact control group. However, in hypophysectomized animals, although plasma testosterone levels increased above that of intact controls, their secondary sex organ weights did not. Moreover, inspite of high circulating hCG levels, the testicular testosterone content and concentration remained suppressed in OeB-treated animals. The reason for such dichotomy of hCG action on OeB-treated animals is not clear at present.


2018 ◽  
Vol 239 (3) ◽  
pp. 303-312 ◽  
Author(s):  
H H Farman ◽  
K L Gustafsson ◽  
P Henning ◽  
L Grahnemo ◽  
V Lionikaite ◽  
...  

The importance of estrogen receptor α (ERα) for the regulation of bone mass in males is well established. ERα mediates estrogenic effects both via nuclear and membrane-initiated ERα (mERα) signaling. The role of mERα signaling for the effects of estrogen on bone in male mice is unknown. To investigate the role of mERα signaling, we have used mice (Nuclear-Only-ER; NOER) with a point mutation (C451A), which results in inhibited trafficking of ERα to the plasma membrane. Gonadal-intact male NOER mice had a significantly decreased total body areal bone mineral density (aBMD) compared to WT littermates at 3, 6 and 9 months of age as measured by dual-energy X-ray absorptiometry (DEXA). High-resolution microcomputed tomography (µCT) analysis of tibia in 3-month-old males demonstrated a decrease in cortical and trabecular thickness in NOER mice compared to WT littermates. As expected, estradiol (E2) treatment of orchidectomized (ORX) WT mice increased total body aBMD, trabecular BV/TV and cortical thickness in tibia compared to placebo treatment. E2 treatment increased these skeletal parameters also in ORX NOER mice. However, the estrogenic responses were significantly decreased in ORX NOER mice compared with ORX WT mice. In conclusion, mERα is essential for normal estrogen signaling in both trabecular and cortical bone in male mice. Increased knowledge of estrogen signaling mechanisms in the regulation of the male skeleton may aid in the development of new treatment options for male osteoporosis.


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