scholarly journals Effect of estrogen treatment on plasma oxytocin and vasopressin in ovariectomized rats.

1979 ◽  
Vol 26 (2) ◽  
pp. 197-205 ◽  
Author(s):  
KEN'ICHI YAMAGUCHI ◽  
TAKAO AKAISHI ◽  
HIDEO NEGORO
Keyword(s):  
Estrogen Treatment ◽  
Ovariectomized Rats

scholarly journals Estrogen modulates the recruitment of myelopoietic cell progenitors in rat through a stromal cell-independent mechanism involving apoptosis

Blood ◽  
1996 ◽  
Vol 87 (7) ◽  
pp. 2683-2692 ◽  
Author(s):  
NK Shevde ◽  
JW Pike
Keyword(s):  
Estrogen Receptor ◽  
Ovarian Function ◽  
Morphological Changes ◽  
Estrogen Treatment ◽  
Ovariectomized Rats ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Protective Effects ◽  
Hematopoietic Stem

Loss of ovarian function leads to a significant increase in the number of bone-resorbing osteoclasts. Estrogen replacement is known to manifest bone protective effects in the treatment of postmenopausal osteoporosis. In the present study, we used ovariectomized rats to examine the effects of estrogen loss at the osteoclast progenitor colony forming unit-granulocyte macrophage (CFU-GM) level. A significant increase in CFU-GM number was observed as early as 7 days following ovariectomy, and correlated directly with an increase in the number of osteoclast-like cells generated in marrow cultures. The increase in CFU-GM following ovariectomy was abrogated in animals that received estrogen treatment in vivo. A similar suppressive effect was observed on CFU-GM number when ovariectomized rat marrow was treated with estrogen in vitro. This effect was blocked in the presence of the estrogen antihormone ICI 164,384. Thus, the data suggest the possibility that estrogen exerts a direct effect on osteoclast progenitors, and does so through the estrogen receptor-mediated mechanism. Ovariectomy also led to an increase in the early hematopoietic stem/progenitor cell population (Thy 1.1+ cells) as determined by FLOW cytometry methods. Morphological changes as well as terminal deoxynucleotidyl transferase assays revealed that estrogen treatment negated growth factor-induced proliferation of these early progenitors by promoting apoptosis. The cellular effects of estrogen in vitro together with the immunocytochemical detection of the estrogen receptor in these cells, strongly support the contention that in addition to osteoclast progenitors such as CFU-GM, earlier hematopoietic progenitors are also unique cellular targets for estrogen action.

Estrogen Treatment Prevents Osteopenia and Depresses Bone Turnover in Ovariectomized Rats*

Endocrinology ◽  
1988 ◽  
Vol 123 (2) ◽  
pp. 681-686 ◽  
Author(s):  
T. J. WRONSKI ◽  
M. CINTRON ◽  
A. L. DOHERTY ◽  
L. M. DANN
Keyword(s):  
Bone Turnover ◽  
Estrogen Treatment ◽  
Ovariectomized Rats

Metabolism of [3H]noradrenaline by the isolated rat uterus

1981 ◽  
Vol 59 (12) ◽  
pp. 1245-1249 ◽  
Author(s):  
Julio Fernández-Pardal ◽  
Martha F. Gimeno ◽  
Alvaro L. Gimeno
Keyword(s):  
Estrogen Treatment ◽  
Ovariectomized Rats ◽  
Noradrenaline Metabolism ◽  
Rat Uterus ◽  
Metabolic Pattern ◽  
Isolated Rat

The metabolism of [3H]noradrenaline by uterine horns from estrous, ovariectomized, and ovariectomized and estrogen-treated rats was explored. Uterine strips are able to take up [3H]noradrenaline and store it for up to 85 min after the isotope incubation. The major compounds retained in the tissue from rats either ovariectomized or during estrus were [3H]noradrenaline and 3H-labelled O-methylated deaminate metabolites. The [3H]3,4-dihydroxyphenylglycol ([3H]DOPEG) and 3,4-dihydroxymandelic acid ([3H]DOMA) fractions were higher in tissues from ovariectomized rats than during estrus. Ovariectomy also increased significantly the spontaneous efflux of [3H]DOPEG and [3H]DOMA. The metabolic pattern of [3H]noradrenaline both in the tissue and in the efflux from ovariectomized rats was changed by estrogen treatment and became similar to those obtained during estrus. These data suggest a possible modulation of the noradrenaline metabolism by estrogens on the isolated rat uterus.

scholarly journals Chronic Estrogen Treatment Modifies Insulin-Induced Insulin Resistance and Hypertension in Ovariectomized Rats

2005 ◽  
Vol 18 (9) ◽  
pp. 1189-1194 ◽  
Author(s):  
D SONG ◽  
E ARIKAWA ◽  
D GALIPEAU ◽  
J YEH ◽  
M BATTELL ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Estrogen Treatment ◽  
Ovariectomized Rats

scholarly journals Estrogen treatment and periodontal disease progression: an experimental study in ovariectomized rats

2012 ◽  
Vol 15 (3) ◽  
Author(s):  
Marianne Spalding ◽  
Priscila Ferreira Amschilnger ◽  
Marcela Almeida Prado ◽  
Ivan Balducci ◽  
Yasmin Rodarte Carvalho
Keyword(s):  
Experimental Study ◽  
Periodontal Disease ◽  
Disease Progression ◽  
Estrogen Treatment ◽  
Ovariectomized Rats

Estrogen treatment to ovariectomized rats modifies morphine-induced behavior

1987 ◽  
Vol 27 (4) ◽  
pp. 611-617 ◽  
Author(s):  
George Nomikos ◽  
Christina Spyraki ◽  
Anna Kazandjian ◽  
Anastasia Sfikakis
Keyword(s):  
Estrogen Treatment ◽  
Ovariectomized Rats

scholarly journals Estrogen Regulation of Neurokinin B Gene Expression in the Mouse Arcuate Nucleus Is Mediated by Estrogen Receptor α

Endocrinology ◽  
2004 ◽  
Vol 145 (2) ◽  
pp. 736-742 ◽  
Author(s):  
Tammy L. Dellovade ◽  
Istvan Merchenthaler
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Postmenopausal Women ◽  
Knockout Mice ◽  
Arcuate Nucleus ◽  
Estrogen Receptor Α ◽  
Estrogen Treatment ◽  
Ovariectomized Rats ◽  
Neurokinin B ◽  
Estrogen Regulation

Abstract Neurokinin B (NKB) gene expression is elevated in the infundibular (arcuate) nucleus of the hypothalamus in postmenopausal women. Estrogen replacement decreases both the number of NKB mRNA-expressing neurons and the level of expression within individual cells. Similarly, NKB gene expression is elevated in ovariectomized rats and reduced after estrogen treatment. The actions of estrogen in the brain can be mediated via either estrogen receptor α (ERα) or estrogen receptor β (ERβ). In the rodent arcuate nucleus (ARC), more ERα- than ERβ-containing cells are present, suggesting that ERα might be directly responsible for estrogen regulation of NKB gene expression. However, an indirect effect via ERβ could not be ruled out. Here we used ERα knockout and ERβ knockout mice to identify the type of ER responsible for mediating estrogen action on NKB gene expression in the ARC. Using in situ hybridization histochemistry, we have found that estrogen treatment significantly reduced NKB gene expression in the ARC of ovariectomized ERβ knockout mice, but had no effect on NKB mRNA levels in ERα knockout mice. These data indicate that ERα mediates the increase in NKB gene expression associated with ovariectomy in rodents and might also be responsible for the increase in NKB in postmenopausal women.

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