scholarly journals Non-steroidal factors in bovine follicular fluid inhibit or facilitate the action of pulsatile administration of GnRH on LH release in the female rat

1999 ◽  
Vol 161 (2) ◽  
pp. 237-243 ◽  
Author(s):  
JA van Dieten ◽  
MN Helder ◽  
C van den Oever ◽  
J de Koning

Using steroid-free bovine follicular fluid (bFF), we studied the action of gonadotrophin surge-inhibiting factor/attenuating factor (GnSIF/AF) on GnRH-induced self-priming in phenobarbital-blocked female rats. For the experiments we used intact rats, short-term (4 h) ovariectomized (OVX) rats and long-term (14 days) OVX rats. In the latter case the rats were injected with 17beta-oestradiol benzoate (OB, 40 micrograms) or vehicle only, 2 or 48 h before the experiment. GnRH (10-50 pmol/kg body weight) was injected intra-arterially in 5 or 15 pulses, respectively 60 or 20 min apart, starting 1 or 4 h after injection of bFF (0.5 or 1.0 ml). In response to 25 pmol/kg GnRH pulses (1/h), we observed no effect in the long-term OVX rats, a minor effect in the intact rats and an enhanced self-priming effect in the short-term OVX rats. Administration of bFF attenuated or even completely inhibited the self-priming process. However, in the case of long-term OVX rats LH release was inhibited only after long-term OB priming. Furthermore, 4 h after administration of bFF, LH release in response to 25 pmol/kg GnRH pulses (3/h) was inhibited transiently in intact rats and long-term OVX rats. The results support the hypothesis of a functional antagonistic action between GnRH and GnSIF/AF. However, when injected 1 h before, bFF facilitated the initial release of the surge-like LH pattern in intact rats in response to 3 pulses/h of GnRH. These results are consistent with an important role of GnSIF/AF and other non-steroidal ovarian factors in the control of both low LH concentrations and the generation of the LH surge. Some genomic action of oestradiol might be a prerequisite for the inhibitory effect of GnSIF/AF on GnRH-induced LH release.

1979 ◽  
Vol 80 (3) ◽  
pp. 303-313 ◽  
Author(s):  
D. K. SARKAR ◽  
G. FINK

The concentration of immunoreactive luteinizing hormone releasing factor (LH-RF) was measured in pituitary stalk blood collected in the afternoon of expected pro-oestrus from rats ovariectomized and given oil, oestradiol benzoate (OB) or progesterone on the morning of dioestrus. Compared with the values in intact rats, LH-RF concentrations were reduced in ovariectomized animals treated with oil or progesterone but not with OB. Administration of progesterone at 12.30 h of expected pro-oestrus reduced the LH-RF concentrations in OB-treated rats; 5α-pregnan-3β-ol-20-one was not as effective as progesterone. The apparent inhibitory effect of progesterone, which was dose-dependent, was not found in long-term adrenalectomized rats, suggesting that it may be due to the production of an inhibitory substance by the adrenal consequent upon steroid administration. These and other data show that oestradiol triggers the spontaneous LH surge by stimulating the release of LH-RF as well as by enhancing pituitary responsiveness. A different mechanism may underlie the reflex surge of LH in rats exposed to constant light for, in these animals, progesterone was found to stimulate LH-RF release.


1986 ◽  
Vol 110 (2) ◽  
pp. 367-373 ◽  
Author(s):  
N. G. Weiland ◽  
C. A. Barraclough ◽  
K. J. Catt

ABSTRACT Considerable differences have previously been found in the hypothalamo-hypophysial responsiveness to oestrogen, depending upon the time between gonad removal and exposure to oestrogen. In the present study a detailed analysis was made of some of the differences which may exist in pituitary LH-releasing hormone (LHRH) receptors and the amount of LH released in response to electrochemical depolarization of the medial preoptic area after 2 or 7 days of oestradiol treatment of long- and short-term gonadectomized male and female rats. The pituitary glands of long-term gonadectomized males and females secreted more LH in response to two pulse injections of LHRH than did short-term gonadectomized rats. The amount of LH released on day 2, however, was equivalent to that secreted after 7 days of oestradiol treatment. Moreover, long-term gonadectomized males and females had equivalent LHRH receptor concentrations, which were greater than those of short-term gonadectomized animals. Peak serum LH concentrations observed after preoptic stimulation were equivalent in short- and long-term castrated rats after 2 days of oestrogen exposure. Serum LH concentrations following preoptic stimulation in short-term gonadectomized males and females were significantly greater on day 7 than on day 2 of oestradiol treatment, whereas in long-term gonadectomized animals the stimulated release of LH was equivalent both in magnitude and time of peak release on both days. These studies demonstrate that the differential effects of oestradiol on LH release on day 2 (no negative feedback) compared with day 7 (both negative and positive feedback exist) are not due to differences in the ability of the pituitary gland to release LH in response to LHRH, nor in the releasable pools of hypothalamic LHRH in long-term gonadectomized rats. Rather, they seem to be due to a refractoriness in some unidentified central nervous process which regulates tonic LH release in gonadectomized rats. J. Endocr. (1986) 110, 367–373


1980 ◽  
Vol 238 (5) ◽  
pp. E458-E462
Author(s):  
L. K. Tang

To determine the factors responsible for the sex difference in luteinizing hormone (LH) response to luteinizing hormone-releasing hormone (LHRH) observed earlier in pituitary cultures, we examined the effects of serum, 17 beta-estradiol, and testosterone on pituitary LHRH-responsiveness and LH synthesis. Cultures prepared from female rats were maintained in medium supplemented with serums. Dextran-coated charcoal (DCC) adsorption of female rat serum reduced, whereas DCC adsorption of male rat serum increased the pituitary LHRH-responsiveness, indicating the existence of stimulatory factor(s) in female rat serum and inhibitory factor(s) in male rat serum. Readdition of testosterone to DCC female rat serum significantly reduced LH release in response to LHRH (78-32% of the control) without affecting total LH content. Readdition of 17 beta-estradiol to DCC female rat serum significantly increased the LH release in response to LHRH, cellular LH content, and 3H-labeled precursor uptake and incorporation into immunoprecipitable LH. These results indicate that the sex difference in LHRH responsiveness may be attributed to the stimulatory effect of 17 beta-estradiol and the inhibitory effect of testosterone on the LH cells.


1982 ◽  
Vol 92 (1) ◽  
pp. 37-42 ◽  
Author(s):  
H. M. A. MEIJS-ROELOFS ◽  
P. KRAMER ◽  
L. GRIBLING-HEGGE

A possible role of 5α-androstane-3α,17β-diol (3α-androstanediol) in the control of FSH secretion was studied at various ages in ovariectomized rats. In the rat strain used, vaginal opening, coincident with first ovulation, generally occurs between 37 and 42 days of age. If 3α-androstanediol alone was given as an ovarian substitute, an inhibitory effect on FSH release was evident with all three doses tested (50, 100, 300 μg/100 g body wt) between 13 and 30 days of age; at 33–35 days of age only the 300 μg dose caused some inhibition of FSH release. Results were more complex if 3α-androstanediol was given in combined treatment with oestradiol and progesterone. Given with progesterone, 3α-androstanediol showed a synergistic inhibitory action on FSH release between 20 and 30 days of age. However, when 3α-androstanediol was combined with oestradiol a clear decrease in effect, as compared to the effect of oestradiol alone, was found between 20 and 30 days of age. Also the effect of combined oestradiol and progesterone treatment was greater than the effect of combined treatment with oestradiol, progesterone and 3α-androstanediol. At all ages after day 20 none of the steroid combinations tested was capable of maintaining FSH levels in ovariectomized rats similar to those in intact rats. It is concluded that 3α-androstanediol might play a role in the control of FSH secretion in the immature rat, but after day 20 the potentially inhibitory action of 3α-androstanediol on FSH secretion is limited in the presence of oestradiol.


2003 ◽  
Vol 95 (6) ◽  
pp. 2614-2623 ◽  
Author(s):  
A. G. Zabka ◽  
G. S. Mitchell ◽  
E. B. Olson ◽  
M. Behan

Age and the estrus cycle affect time-dependent respiratory responses to episodic hypoxia in female rats. Respiratory long-term facilitation (LTF) is enhanced in middle-aged vs. young female rats ( 72 ). We tested the hypothesis that phrenic and hypoglossal (XII) LTF are diminished in acyclic geriatric rats when fluctuating sex hormone levels no longer establish conditions that enhance LTF. Chronic intermittent hypoxia (CIH) enhances LTF ( 41 ); thus we further predicted that CIH would restore LTF in geriatric female rats. LTF was measured in young (3-4 mo) and geriatric (20-22 mo) female Sasco Sprague-Dawley rats and in a group of geriatric rats exposed to 1 wk of nocturnal CIH (11 vs. 21% O2 at 5-min intervals, 12 h/night). In anesthetized, paralyzed, vagotomized, and ventilated rats, time-dependent hypoxic phrenic and XII responses were assessed. The short-term hypoxic response was measured during the first of three 5-min episodes of isocapnic hypoxia (arterial Po2 35-45 Torr). LTF was assessed 15, 30, and 60 min postepisodic hypoxia. Phrenic and XII short-term hypoxic response was not different among groups, regardless of CIH treatment ( P > 0.05). LTF in geriatric female rats was smaller than previously reported for middle-aged rats but comparable to that in young female rats. CIH augmented phrenic and XII LTF to levels similar to those of middle-aged female rats without CIH ( P < 0.05). The magnitude of phrenic and XII LTF in all groups was inversely related to the ratio of progesterone to estradiol serum levels ( P < 0.05). Thus CIH and sex hormones influence the magnitude of LTF in geriatric female rats.


1992 ◽  
Vol 70 (7) ◽  
pp. 963-969 ◽  
Author(s):  
Gabriela T. Pérez ◽  
Marta E. Apfelbaum

The purpose of the present experiments was to examine the short- and long-term effects of estradiol-17β (E2), progesterone (P), and 5α-dihydrotestosterone (DHT), alone and in combination, on the gonadotrophin-releasing hormone (GnRH)-induced luteinizing hormone (LH) secretion, using an ovariectomized rat pituitary cells culture model. After 72 h in steroid-free medium, pituitary cells were further cultured for 24 h in medium with or without E2 (1 nM), P (100 nM), or DHT (10 nM). Cultures were then incubated for 5 h in the absence or presence of 1 nM GnRH with or without steroids. LH was measured in the medium and cell extract by radioimmunoassay. The results show that the steroid hormones exert opposite effects on the release of LH induced by GnRH, which seems to be dependent upon the length of time the pituitary cells have been exposed to the steroids. In fact, short-term (5 h) action of E2 resulted in a partial inhibition (64% of control) of LH release in response to GnRH, while long-term (24 h) exposure enhanced (158%) GnRH-induced LH release. Similar results were obtained with DHT, although the magnitude of the effect was lower than with E2. Conversely, P caused an acute stimulatory action (118%) on the LH released in response to GnRH and a slightly inhibitory effect (90%) after chronic treatment. GnRH-stimulated LH biosynthesis was also influenced by steroid treatment. Significant increases in total (cells plus medium) LH were observed in pituitary cells treated with E2 or DHT. While the stimulatory effect of E2 was evident after both acute (133%) and chronic (119%) treatment, that of DHT appears to be exerted mainly after long-term priming (118%). These results suggest that the steroids modulate GnRH-induced LH secretion by acting on both synthesis and release of LH. On the other hand, total hormone content was not affected by P. The acute (5 h) effects of E2, P, and DHT on the GnRH response in E2-primed (24 h) cells during a short-term incubation, were also tested. Addition of P to the pituitary cells primed with E2 led to an acute potentiation of the stimulatory effect of E2 on GnRH-induced LH release and total content. Conversely, the augmentative E2 effect on pituitary responsiveness to GnRH was abolished by DHT. Taken together, these findings suggest that the physiological significance of the stimulatory action of progesterone could be to define the final magnitude of the LH preovulatory surge, while the inhibition by DHT could be required to limit the LH surge to that day of proestrus.Key words: luteinizing hormone, gonadotrophin-releasing hormone, steroid hormones, cultured pituitary cells.


1994 ◽  
Vol 76 (4) ◽  
pp. 1540-1547 ◽  
Author(s):  
D. J. Prezant ◽  
B. Richner ◽  
T. K. Aldrich ◽  
D. E. Valentine ◽  
E. I. Gentry ◽  
...  

The effects of long-term undernutrition (10 wk) on diaphragm contractility, fatigue, and fiber type proportions were studied in male and female rats. Contractility and fatigue resistance indexes were measured in an in vitro diaphragm costal strip preparation by using direct stimulation at 37 degrees C. Undernutrition allowed for continued growth in males and females but with substantial reductions in weight gain. Relative to control rats of the same sex, final weights were significantly lower in undernourished males (74 +/- 3%) than females (90 +/- 5%), but weight gain was not significantly different between undernourished males (58 +/- 5%) and females (60 +/- 3%). Only in males did undernutrition significantly reduce costal diaphragm weight (to 77 +/- 5% of control). Diaphragm forces, normalized for cross-sectional area, were not significantly different from male or female control values. Fatigue resistance indexes (fatigue/baseline force) were increased at all stimulation frequencies in undernourished males but not in undernourished females. Costal diaphragm atrophy, involving types I and II fibers, occurred in undernourished males but not in undernourished females. In conclusion, despite long-term undernutrition reducing weight gain to similar levels in males and females (relative to control), there was excellent preservation of diaphragm weight, function, and structure in females but, although diaphragm atrophy occurred, there was preserved contractility and increased fatigue resistance in males.


1997 ◽  
Vol 154 (2) ◽  
pp. 241-248 ◽  
Author(s):  
C Aurich ◽  
J Lange ◽  
H-O Hoppen ◽  
J E Aurich

Abstract The aim of this study was to investigate the influence of oestradiol, melatonin and season on the opioid regulation of LH and prolactin release. Effects of the opioid antagonist naloxone (0·5 mg/kg) on LH and prolactin secretion were determined in ovariectomized pony mares. In experiment 1, mares in January (n=6) were pretreated with oestradiol benzoate (5 μg/kg) for 20 days. In experiment 2, beginning in May, mares (n=7) received melatonin (15 mg) for 15 days and subsequently a combination of melatonin plus oestradiol for 20 days. In experiment 3, beginning in May, mares (n=6) were pretreated with oestradiol for 30 days, left untreated for 12 days and then given melatonin for 35 days. In all experiments the animals were injected with the opioid antagonist naloxone and saline on 2 consecutive days prior to treatment. In experiment 1, animals received naloxone and saline on days 10 and 11 and 20 and 21 following oestradiol treatment. In experiment 2, naloxone and saline were administered on days 15 and 16 following melatonin treatment and on days 10 and 11 and 20 and 21 of melatonin plus oestradiol treatment. In experiment 3, the animals received naloxone and saline on days 10 and 11, 20 and 21 and 30 and 31 of oestradiol treatment, prior to melatonin treatment and on days 15 and 16, 25 and 26 and 35 and 36 following melatonin. In January (experiment 1), naloxone evoked a significant (P<0·05) LH release at all times, however the LH increment in response to naloxone increased during oestradiol pretreatment (P<0·05) During the breeding season (experiments 2 and 3), naloxone induced a significant (P<0·05) increase in plasma LH concentrations when mares had not been pretreated with oestradiol or melatonin and after oestradiol pretreatment. Basal LH concentrations and the LH increment in response to naloxone increased significantly (P<0·05) during the 30-day oestradiol pretreatment. Melatonin decreased the naloxone-induced LH release and the LH release in response to naloxone and saline no longer differed after 25 and 35 days of melatonin pretreatment. When melatonin was given together with oestradiol for 20 days, again a significant (P<0·05) LH release in response to naloxone occurred. Prolactin release was significantly (P<0·05) increased by naloxone when mares had been pretreated with only melatonin. The opioid antagonist did not affect prolactin release in mares that had not been pretreated or received oestradiol either alone or in combination with melatonin. In conclusion, in long-term ovariectomized mares, opioids inhibit LH secretion independent from ovarian factors. This opioid inhibition of LH secretion is enhanced by oestradiol and reduced by melatonin. Although short-term melatonin treatment in-activates the opioid regulation of LH release, a prolonged influence of melatonin as occurs in winter does not prevent activation of the opioid system. This indicates that effects of melatonin on the opioid regulation of LH release change with time. An opioid inhibition of prolactin secretion is activated by melatonin given for 15–35 days but is lost under the prolonged influence of a short-day melatonin signal in winter. Journal of Endocrinology (1997) 154, 241–248


1977 ◽  
Vol 86 (2) ◽  
pp. 263-272 ◽  
Author(s):  
J. Kronibus ◽  
W. Wuttke

ABSTRACT Female rats were ovariectomized (ovx), adrenalectomized (adx) or both (adx-ovx) on day 8 after birth. The serum gonadotrophin concentrations on day 15 were higher in ovx and adx-ovx rats than in sham-operated or untreated controls of the same age. Intact animals on day 15 had higher LH and FSH levels compared with adult, dioestrous levels, and a number of LH peaks were observed. After partial separation of oestradiol (LH 20 column chromatography) from other lipid substances which interfere with the radioimmunoassay for oestradiol, levels of oestradiol were undetectable in ovx and in adx-ovx animals on day 15 but concentrations were relatively high in intact or adx rats. To test whether the high gonadotrophin concentrations in 15-day-old intact rats were due to a positive feedback action of oestradiol, silastic tubes containing different amounts of oestradiol were implanted on day 8 at the time of adrenalectomy and ovariectomy. The mean serum LH and FSH concentrations were increased on day 15 in those animals in which silastic tube implantation resulted in physiological oestradiol levels. These elevated gonadotrophin values were due to a number of peak levels. Injection of 600 μg progesterone on day 15, 8 h before decapitation resulted in high FSH levels in all the implanted animals, whereas LH levels were still variable from one animal to another. This situation is very similar to that in intact control rats and it is concluded that the hypothalamo-pituitary axis in 15-day-old female rats reacts to an oestrogenic stimulus followed by a progestational reaction as does the adult "gonadostat". This would account for the premature, pre-ovulatory type of LH peaks.


1984 ◽  
Vol 103 (3) ◽  
pp. 317-325
Author(s):  
A. K. Brar ◽  
G. Fink

ABSTRACT The effects of catechol oestradiol and catechol oestrone on the release of LH and prolactin were investigated in immature male and female Wistar rats. In male rats both catechol oestradiol and catechol oestrone significantly increased the plasma concentration of LH, and catechol oestradiol but not catechol oestrone significantly increased the plasma concentration of prolactin and decreased the pituitary concentration of LH. The parent oestrogens, oestradiol-17β and oestrone, had no effect on plasma LH concentrations, but both increased significantly the plasma concentration of prolactin, and oestrone but not oestradiol-17β increased the pituitary concentration of LH. In immature female rats, catechol oestradiol inhibited the surge of LH and the increase in uterine weight induced by injecting pregnant mare serum gonadotrophin (PMSG). The injection of oestrone induced an increase in the plasma concentration of LH which was about nine times greater than that produced by oestradiol-17β. There were no significant differences in the effects of these steroids on plasma prolactin concentration. These results (i) confirm that in the immature male rat catechol oestrogens can stimulate LH release and show that catechol oestradiol can increase prolactin release, (ii) show that catechol oestradiol can inhibit the stimulatory effects of PMSG on LH release and uterine weight in the immature female rat, and (iii) demonstrate that oestrone can stimulate LH release in the immature female rat. J. Endocr. (1984) 103, 317-325


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