scholarly journals Time Course of Serum FSH Suppression in Ovariectomized Rats Injected with Porcine Follicular Fluid (Folliculostatin): Effect of Estradiol Treatment

1979 ◽  
Vol 20 (5) ◽  
pp. 1093-1098 ◽  
Author(s):  
Constance S. Campbell ◽  
Neena B. Schwartz
1987 ◽  
Vol 35 (6) ◽  
pp. 657-662 ◽  
Author(s):  
J P Holt ◽  
E Rhe

Lactate dehydrogenase (LDH; EC 1.1.1.27), citrate synthase (CS; EC 4.1.3.7), and beta-hydroxyacyl-CoA-dehydrogenase (beta-OH-acyl-CoA-DH; EC 1.1.1.35) activities were determined in each of the three major cell types of rat uterus, i.e., epithelial, stromal, and smooth muscle, using quantitative microanalytical techniques. Adult ovariectomized rats were treated with 17-beta-estradiol to determine the time course and dose response (0.025-50 micrograms/300-g rat) effect of estrogen on enzyme activity of each type of uterine cell. The use of "oil well" and enzyme-cycling microtechniques to determine the time course and the dose responses of enzyme activity changes required microassays involving 1595 microdissected single cell specimens. Estradiol treatment increased epithelial LDH, CS and beta-OH-acyl-CoA-DH activity but had no effect on these enzymes in the stroma or in smooth muscle cells. The estradiol-stimulated peak enzyme activities on Day 4 in the intervention group are compared with those in the ovariectomized rat controls as follows: LDH, 44.5 +/- 3.5 vs 22.3 +/- 3.9; CS, 3.5 +/- 0.2 vs 1.5 +/- 0.6; beta-OH-acyl-CoA-H, 3.5 +/- 0.32 vs 2.2 +/- 0.2 (mean +/- standard deviation; mol/kg/hr). Stromal cell activities (LDH, 7.4 +/- 1.0; CS, 1.2 +/- 0.2; beta-OH-acyl-CoA-DH, 0.9 +/- 0.1) were significantly lower than epithelial cell levels and were similar to smooth muscle levels. Therefore, even in the ovariectomized animal epithelial cells have markedly higher metabolic activity compared with adjacent cells. The enzyme activities are expressed as moles of substrate reacting per kilogram of dry weight per hour. All three enzymes exhibited a 17-beta-estradiol-induced dose response between 0.025-0.15 micrograms/300-g rat. The three enzymes studied all had similar response patterns to estrogen. The effect of estradiol was restricted to epithelial cells, with enzyme activities increasing to maximal levels after approximately 96 hr of hormone treatment. This study therefore not only confirms the specific and differential metabolic responses of uterine cells to estradiol treatment, but clearly demonstrates that marked metabolic differences exist between epithelial cells and stromal or smooth muscle uterine cells.


2011 ◽  
Vol 103 (3-4) ◽  
pp. 261-267 ◽  
Author(s):  
Nora S. Graves ◽  
Heather Hayes ◽  
Liming Fan ◽  
Kathleen S. Curtis

1982 ◽  
Vol 101 (4) ◽  
pp. 501-506 ◽  
Author(s):  
A. A. J. Jenner ◽  
J. de Koning ◽  
G. P. van Rees

Abstract. Inhibin-like activity in steroid-free bovine follicular fluid (bFF) is demonstrated using an in vitro technique with hemi-pituitary glands from intact female (second day of dioestrus) and ovariectomized rats: synthesis as well as basal release of FSH, but not of LH, are inhibited profoundly. The results confirm and extend data from other investigators on the action of inhibin-like material. The effect of the inhibin-like activity is shown to be reversible, as synthesis and the rise of basal release are restored when bFF is withdrawn from the incubation medium. Synthesis of FSH seems to be inhibited earlier than basal release, and it is suggested that the inhibin-like material acts only directly on FSH synthesis. Some possibilities of the mechanisms of action of inhibin-like activity are discussed.


2001 ◽  
Vol 281 (3) ◽  
pp. R738-R746 ◽  
Author(s):  
Lisa A. Eckel ◽  
Nori Geary

The steroid hormone estradiol decreases meal size by increasing the potency of negative-feedback signals involved in meal termination. We used c-Fos immunohistochemistry, a marker of neuronal activation, to investigate the hypothesis that estradiol modulates the processing of feeding-induced negative-feedback signals within the nucleus of the solitary tract (NTS), the first central relay of the neuronal network controlling food intake, and within other brain regions related to the control of food intake. Chow-fed, ovariectomized rats were injected subcutaneously with 10 μg 17-β estradiol benzoate or sesame oil vehicle on 2 consecutive days. Forty-eight hours after the second injections, 0, 5, or 10 ml of a familiar sweet milk diet were presented for 20 min at dark onset. Rats were perfused 100 min later, and brain tissue was collected and processed for c-Fos-like immunoreactivity. Feeding increased the number of c-Fos-positive cells in the NTS, the paraventricular nucleus of the hypothalamus (PVN), and the central nucleus of the amygdala (CeA) in oil-treated rats. Estradiol treatment further increased this response in the caudal, subpostremal, and intermediate NTS, which process negative-feedback satiation signals, but not in the rostral NTS, which processes positive-feedback gustatory signals controlling meal size. Estradiol treatment also increased feeding-induced c-Fos in the PVN and CeA. These results indicate that modest amounts of food increase neuronal activity within brain regions implicated in the control of meal size in ovariectomized rats and that estradiol treatment selectively increases this activation. They also suggest that estradiol decreases meal size by increasing feeding-related neuronal activity in multiple regions of the distributed neural network controlling meal size.


Endocrinology ◽  
2012 ◽  
Vol 154 (2) ◽  
pp. 842-852 ◽  
Author(s):  
Christine F. Witty ◽  
Layne P. Gardella ◽  
Maria C. Perez ◽  
Jill M. Daniel

We previously demonstrated that aged ovariectomized rats that had received prior estradiol treatment in middle age exhibited enhanced spatial memory and increased levels of estrogen receptor (ER)-α in the hippocampus long after estradiol treatment was terminated. The implication for cognition of increased levels of ERα resulting from prior estradiol exposure is unknown. In the absence of estrogens, growth factors, including IGF-I, can induce ERα-mediated transcription through ligand-independent mechanisms. Our current goal was to determine whether IGF-I mediates the ability of short-term exposure to estradiol to exert long-term effects on cognition and the hippocampus of aging females. Ovariectomized middle-aged rats were implanted with estradiol or cholesterol vehicle capsules. After 40 days, all capsules were removed and drug treatments were initiated. Half of each hormone treatment group received chronic intracerebroventricular delivery of the IGF-I receptor antagonist JB1, and the other half received artificial cerebrospinal fluid vehicle. Rats were tested on a spatial memory radial-arm maze task and hippocampi were immunostained for proteins of interest by Western blotting. As expected, previous treatment with estradiol enhanced spatial memory and increased levels of ERα in the hippocampus. JB1 reversed these effects. Previous treatment with estradiol resulted in lasting increases in levels of IGF-I receptors and phosphorylation of ERK/MAPK, a downstream signaling molecule of both ERα and IGF-I receptors, and increased levels of the ERα-regulated protein, choline acetyltransferase. JB1 blocked effects on ERK/MAPK and choline acetyltransferase. Results indicate that activation of IGF-I receptors is necessary for prior estradiol exposure to exert lasting impact on the hippocampus and memory.


1983 ◽  
Vol 99 (1) ◽  
pp. 1-8 ◽  
Author(s):  
T. R. Koiter ◽  
G. C. J. van der Schaaf-Verdonk ◽  
H. Kuiper ◽  
N. Pols-Valkhof ◽  
G. A. Schuiling

The effects of steroid-free bovine follicular fluid (bFF) and sodium phenobarbitone on spontaneous LH releasing hormone (LHRH)-induced secretion of FSH and LH were studied in ovariectomized rats. Luteinizing hormone releasing hormone was administered by infusion to rats anaesthetized with phenobarbitone. Bovine follicular fluid reduced FSH release and synthesis. Luteinizing hormone release remained unaffected after bFF treatment. Phenobarbitone reduced both FSH and LH release. The observed suppressive effects of bFF and phenobarbitone on FSH secretion were additive, suggesting that the basal release of FSH has an LHRH-dependent and an LHRH-independent component. Furthermore, bFF did not affect pituitary responsiveness of LH secretion to LHRH and reduced the responsiveness of FSH secretion only when administered some time before the LHRH challenge. The present observations support the view that in the ovariectomized rat the pituitary gland is the only site of action of inhibin-like activity as present in bFF.


2012 ◽  
Vol 1470 ◽  
pp. 1-10 ◽  
Author(s):  
Dulce A. Velázquez-Zamora ◽  
David González-Tapia ◽  
Myrna M. González-Ramírez ◽  
Mario E. Flores-Soto ◽  
Eduardo Vázquez-Valls ◽  
...  

1987 ◽  
Vol 113 (3) ◽  
pp. 449-455 ◽  
Author(s):  
W. J. de Greef ◽  
G. A. M. Eilers ◽  
J. de Koning ◽  
B. Karels ◽  
F. H. de Jong

ABSTRACT Intraperitoneal administration of bovine follicular fluid (bFF) decreased plasma concentrations of FSH in ovariectomized rats after 2–3 h, while plasma LH and prolactin were unaffected. In untreated ovariectomized animals the concentrations of these hormones were found to show pulsatile variations. Concomitant occurrence of peak values of LH and FSH was found in about 40% of the pulses. No pulses of FSH were observed after i.p. treatment with bFF or partly purified preparations of inhibin from bFF, but the pulsatile release of LH and prolactin remained similar. Infusion of bFF into the lateral ventricle of the brain did not alter the concentrations of FSH, whereas administration of bFF into the pituitary gland diminished the plasma concentrations of FSH. Anaesthesia (urethane plus xylazine) did not prevent the occurrence of the pulses of FSH and LH, but it reduced the pulse amplitude and clearance. During this anaesthesia, the concentrations of LHRH in the hypophysial stalk plasma decreased by 30% after administration of bFF, but did not alter after treatment with partly purified preparations of inhibin. It is concluded that the inhibin-like activity in bFF suppresses pulsatile FSH secretion in ovariectomized rats by an action on the pituitary gland, but has no effect on the pulsatile release of LH and prolactin. J. Endocr. (1987) 113, 449–455


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