Estrogenic Induction of Spermatogenesis in the Hypogonadal Mouse*

Ebling, Francis J. P.; An, Bo; Cronin, Anna; Ford, Hazel; Kerr, J. B.

doi:10.1210/endo.141.8.7596

Cited by 105 publications

(47 citation statements)

References 43 publications

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“…adult male rats that received increasing doses of estradiol showed significant decreases in circulating concentrations of FSH and LH, which lead to subsequent reductions in serum and testicular testosterone levels [57]. Surprisingly, the authors of this study also noted a stimulatory effect of low doses of estradiol on FSH, as was demonstrated by studies in the neonate [58], and in adult hypogonadal mice given physiological doses of estradiol [59]. Thus, estrogens can participate in both negative and positive effects on the pituitary in male rodents.…”

Section: Discussionsupporting

confidence: 48%

17β-estradiol effect on testicular β-endorphin expression in Psammomys obesus

Madani¹,

Moudilou²,

Exbrayat³

et al. 2015

Folia Histochem Cytobiol.

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Introduction. Testicular function in the sand rodent Psammomys obesus is subjected to seasonal alternations with a trigger of spermatogenesis in winter and a total quiescence which extends from late spring to summer. The aim of this study was to investigate the distribution of b-endorphin in the testis at the period of winter sexual activity and at its summer regression, and assess the effect of 17b-estradiol treatment on testicular morphology and b-endorphin expression. Material and methods. The adult males were grouped into 4 groups (rest group, sexually active group, rest treated with 17b-estradiol group and controls at sexual rest injected with olive oil, n = 5 in each group). Using anti-serum against b-endorphin, we studied its testicular expression by Western blot and cellular location by immunohistochemical (IHC) method, respectively. Results. We detected by Western blot a peptide of 3.5 kDa molecular weight corresponding to b-endorphin only in sexually resting and control males. The 17b-estradiol treatment induced a clear reduction in the b-endorphin band expression compared with the latter. These results were confirmed by the IHC analysis since b-endorphin was only observed in the testis at sexual rest and in controls, in majority of seminiferous tubules at the level of germ cells. The intensity of IHC labeling was significantly different between spermatogonia and spermatocytes I or round spermatids which revealed the strongest labeling. The intense immunoreactivity was also located in Leydig cells and highly significantly varied compared to the germ cells. The 17b-estradiol treatment decreased significantly the b-endorphin signal in germ cells but not in Leydig cells. Conclusion. The 17b-estradiol treatment induces a repressive effect on seasonal testicular endorphinergic system in P. obesus and this action targets exclusively the germ cells.

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Section: Discussionsupporting

confidence: 48%

17β-estradiol effect on testicular β-endorphin expression in Psammomys obesus

Madani¹,

Moudilou²,

Exbrayat³

et al. 2015

Folia Histochem Cytobiol.

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“…However, this is paradoxical since estradiol inhibits FSH secretion in GnRH intact animals [Ebling et al 2000;Finkelstein et al 1991;Pitteloud et al 2008] suggesting that the stimulatory effect of estrogen on FSH secretion is unique to animals lacking GnRH signaling. While it is possible serum FSH concentrations were increased in our animals, we believe this to be unlikely because our animals had functional GnRH signaling and the dynamics of FSH synthesis and secretion.…”

Section: Discussionmentioning

confidence: 99%

Alterations in the estrogen environment of the testis contribute to declining sperm production in aging rats

Clarke

Pearl

2014

Systems Biology in Reproductive Medicine

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Testicular function, specifically, production of testosterone by Leydig cells, diminishes during aging. Estradiol is also produced by the testis and potentially acts in an autocrine or paracrine manner to help regulate spermatogenesis. However, changes in estradiol concentration or receptor expression within the testis during aging remain unclear. This study was designed to test the hypothesis that the estrogen environment of the testis is altered during aging and that these changes are associated with declining sperm production. Sprague Dawley rats were examined at three, 15, 18, and 21 months of age to detail changes in sperm production and testicular concentration of testosterone and estradiol; five rats were used at three and 21 months and three rats were used at 15 and 18 months. Daily sperm production declined 49% from 15 to 21 months of age. Testicular concentrations of estradiol declined 53% from 15 to 21 months of age; testosterone concentrations were not significantly different. These results suggest that declines in intra-testicular estradiol may contribute to declining sperm production. We further tested our hypothesis by treating rats once every third day with a subcutaneous injection of estradiol valerate (1 µg/kg) from 15 to 18 months of age. Estradiol was increased 54% in treated animals while testosterone was unaffected. Estrogen receptor alpha (ESR1) expression was significantly reduced from 15 to 18 months and expression in estrogen-treated animals was significantly higher than age-matched controls. Additionally, ESR1 expression in 18 month treated animals was not different from 15 months of age. Importantly, daily sperm production in 18 month treated animals was 22% higher than age-matched controls; thus, treatment prevented approximately half of the decline observed in control animals. Collectively, our results suggest that estrogen is involved in maintaining optimum spermatogenesis in adult rats and that estrogen treatment may attenuate the age-associated loss in sperm production.

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“…The osmotic minipumps can deliver a constant dose of E2 with a plasma profile similar to that of a slow release pellet, which is commonly used in long-term in vivo studies (Fara & Urquhart 1984, Ebling et al 2000. The major advantage of using osmotic minipumps is that they can be connected to a brain infusion cannula, enabling continuous long term i.c.v.…”

Section: Discussionmentioning

confidence: 99%

Investigation of central versus peripheral effects of estradiol in ovariectomized mice

Andersson¹,

Islander²,

Egecioglu³

et al. 2005

Journal of Endocrinology

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It is generally believed that estrogens exert their bone sparing effects directly on the cells within the bone compartment. The aim of the present study was to investigate if central mechanisms might be involved in the bone sparing effect of estrogens. The dose-response of central (i.c.v) 17 -estradiol (E2) administration was compared with that of peripheral (s.c.) administration in ovariectomized (ovx) mice. The dose-response curves for central and peripheral E2 administration did not differ for any of the studied estrogen-responsive tissues, indicating that these effects were mainly peripheral. In addition, ovx mice were treated with E2 and/or the peripheral estrogen receptor antagonist ICI 182,780. ICI 182,780 attenuated most of the estrogenic response regarding uterus weight, retroperitoneal fat weight, cortical BMC and trabecular bone mineral content (P<0·05). These findings support the notion that the primary target tissue that mediates the effect of E2 on bone is peripheral and not central.

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Estrogenic Induction of Spermatogenesis in the Hypogonadal Mouse*

Cited by 105 publications

References 43 publications

17β-estradiol effect on testicular β-endorphin expression in Psammomys obesus

17β-estradiol effect on testicular β-endorphin expression in Psammomys obesus

Alterations in the estrogen environment of the testis contribute to declining sperm production in aging rats

Investigation of central versus peripheral effects of estradiol in ovariectomized mice

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