Suppression of LH secretion by oestradiol, dihydrotestosterone and trenbolone acetate in the acutely castrated bull

1984 ◽  
Vol 100 (1) ◽  
pp. 107-112 ◽  
Author(s):  
T. W. Gettys ◽  
M. J. D'Occhio ◽  
D. M. Henricks ◽  
B. D. Schanbacher
Keyword(s):  
Feedback Control ◽  
Pituitary Gland ◽  
Treated Group ◽  
Primary Site ◽  
Trenbolone Acetate ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Lh Releasing Hormone ◽  
Lh Secretion

ABSTRACT Twenty acutely castrated bulls were used to investigate the role of androgenic and oestrogenic steroids in the feedback control of LH secretion. The effects of 5α-dihydrotestosterone (DHT) or the growth stimulants trenbolone acetate (TBA) or oestradiol-17β (OE2) on serum LH secretory profiles were measured. In addition, pituitary LH responses to exogenous LH releasing hormone (LHRH) were determined to differentiate between hypothalamic and pituitary sites of steroid action. At the time of castration, two groups of animals were given implants of either 45 mg OE2 or 200 mg TBA. Another group received equivalent to 30 mg daily injections of DHT. Control steers showed an increase in LH from 2·4 ± 0·5 (s.e.m.) μg/l to 7·0 ± 0·5 μg/l during the week after castration. Treatment with DHT and TBA prevented the post-castration rise in serum LH. In contrast, steers given implants of OE2 showed a significantly greater increase in LH than controls 1 day after castration, but by day 5 LH declined in the OE2-treated group to precastration values. Five weeks after castration control steers secreted LH in pulses at intervals of 40–50 min and with an amplitude of 4·2± 0·4 μg/l. Pulses were not detected in the LH profiles of the steroid-treated steers. Dihydrotestosterone and TBA significantly reduced pituitary LH responses to exogenous LHRH, whereas steers receiving OE2 showed LH responses to LHRH which were similar to those observed in castrated controls. These results support the hypothesis that androgenic and oestrogenic components participate separately in the feedback control of LH secretion in the bull. A similar LH response to exogenous LHRH in control and OE2-treated animals suggests that the primary site of oestrogen feedback is at the level of the hypothalamus. Conversely, the small LH response to LHRH in androgen-treated animals suggests that androgen feedback is, in part, imposed at the level of the pituitary gland. Interestingly, LH secretion is regulated by dosages of androgenic and oestrogenic steroids which are available commercially as growth stimulants for cattle. J. Endocr. (1984) 100, 107–112

LUTEINIZING HORMONE RELEASING HORMONE-INDUCED RELEASE OF LUTEINIZING HORMONE FROM PITUITARY EXPLANTS OF COWS KILLED BEFORE OR AFTER OESTRADIOL TREATMENT

1981 ◽  
Vol 88 (1) ◽  
pp. 17-25 ◽  
Author(s):  
E. M. CONVEY ◽  
J. S. KESNER ◽  
V. PADMANABHAN ◽  
T. D. CARRUTHERS ◽  
T. W. BECK
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Lh Surge ◽  
Releasing Hormone ◽  
Oestradiol Treatment ◽  
Readily Releasable Pool ◽  
Serum Lh ◽  
Pituitary Glands ◽  
Lh Rh ◽  
Lh Releasing Hormone

In ovariectomized heifers, oestradiol decreases concentrations of LH in serum for approximately 12 h after which LH is released in a surge comparable in size and duration to the preovulatory surge. Using this model, we measured LH release induced by LH releasing hormone (LH-RH) from pituitary explants taken from ovariectomized heifers before or after an oestradiol-induced LH surge. These changes were related to changes in LH concentrations in serum and pituitary glands and hypothalamic LH-RH content. Twenty Holstein heifers were randomly assigned to one of four treatment groups to be killed 0, 6, 12, or 24 h after the injection of 500 μg oestradiol-17β. Jugular blood was collected at −2, −1 and 0 h then at intervals of 2 h until slaughter. Pituitary glands were collected and ≃2 mm3 explants were exposed to 4 ng LH-RH/ml medium for 30 min (superfusion) or 4 ng LH-RH/ml medium for 2 h in Erlenmeyer flasks. Levels of LH were measured in the medium. Hypothalami, collected at autopsy, were assayed for LH-RH content. To determine pituitary LH content, an additional 15 ovariectomized heifers were killed, five each at 0, 12 and 24 h after the injection of 500 μg oestradiol. In both groups of heifers, oestradiol reduced serum LH concentrations to ≃ 1 ng/ml, a level which persisted for 12 h, when LH was released in a surge. Pituitary sensitivity to LH-RH was increased at 6 and 12 h after the injection of oestradiol, but was markedly decreased at 24 h, i.e. after the LH surge. Despite this twofold increase in capacity of the pituitary gland to release LH in response to LH-RH, pituitary LH content did not change during 12 h after oestradiol treatment. However, LH content decreased after the LH surge and this decrease was associated with a decrease in pituitary responsiveness to LH-RH. Hypothalamic LH-RH content was not altered by these treatments. We have interpreted our results as evidence that oestradiol exerts a positive feedback effect on the pituitary gland of ovariectomized heifers such that pituitary sensitivity to LH-RH is increased twofold by the time the LH surge is initiated. In addition, oestradiol causes a transitory inhibition of LH-RH release as shown by the fact that serum LH concentrations remained low during the interval from injection of oestradiol until the beginning of the LH surge despite the fact that pituitary sensitivity to LH-RH is increased at this time. Depletion of a readily releasable pool of pituitary LH may be the mechanism by which the LH surge is terminated.

Evidence of gonadal steroid-independent changes in activity of the central LH-releasing hormone pulse generator in developing bull calves

1986 ◽  
Vol 111 (1) ◽  
pp. 67-73 ◽  
Author(s):  
M. J. D'Occhio ◽  
D. R. Gifford ◽  
T. Weatherly ◽  
B. P. Setchell
Keyword(s):  
Pulse Generator ◽  
Age Groups ◽  
Pulse Frequency ◽  
Releasing Hormone ◽  
Age Related ◽  
Bull Calves ◽  
Serum Lh ◽  
Transient Rise ◽  
Lh Releasing Hormone ◽  
Lh Secretion

ABSTRACT To ascertain whether temporal changes in activity of the hypothalamo-pituitary axis in prepubertal bulls may occur independently of shifts in sensitivity to steroid feedback, the acute post-castration rise in serum gonadotrophins was monitored in bull calves castrated at monthly intervals from 4 to 9 months of age. Since a major feature of the gonadotrophin profiles of developing bulls is a change in LH pulse frequency early in life, pulsatile LH secretion after castration was used as an index of activity of the central LH-releasing hormone (LHRH) pulse generator. Relative to the day of castration (day 0) bull calves (n = 4) were bled at 20-min intervals for 8 h on day −3 and at 10-min intervals for 4 h on days 3, 5 and 7. During the first week after castration, 4-month-old bulls showed a higher (P<0·05) frequency of LH pulses compared with bulls at 8 and 9 months (1·13, 0·88 and 0·75 pulses/h respectively; pooled s.e.m.= 0·13). Mean LH levels before castration were higher (P<0·05) in 4-month-old bulls than in bulls at 7, 8 and 9 months (0·92, 0·37, 0·31, 0·38 μg/l respectively; pooled s.e.m. = 0·12). After castration mean LH levels did not differ with age. Mean FSH levels did not differ among age groups either before or after castration. Increased serum LH levels in 4-month-old bulls confirmed the transient rise in LH secretion that occurs at this time in developing bull calves. Age-related differences in LH pulse frequency observed after castration suggested that in prepubertal bulls changes in activity of the central LHRH pulse generator can occur independently of steroid feedback mechanisms. J. Endocr. (1986) 111, 67–73

The role of microfilaments in the priming effect of LH-releasing hormone: an ultrastructural study using cytochalasin B

1985 ◽  
Vol 106 (2) ◽  
pp. 211-NP ◽  
Author(s):  
C. E. Lewis ◽  
J. F. Morris ◽  
G. Fink
Keyword(s):  
Adult Female ◽  
Ultrastructural Study ◽  
Incubation Medium ◽  
Priming Effect ◽  
Cytochalasin B ◽  
Secretory Granules ◽  
Releasing Hormone ◽  
Lh Releasing Hormone ◽  
Lh Secretion

ABSTRACT We have investigated the possibility that microfilaments are involved in the priming effect of LH-releasing hormone (LHRH) by ultrastructural morphometry of hemipituitary glands from adult female mice. Glands incubated for 2 consecutive hours with 8·5 nmol LHRH/1 responded with a marked increase in the amount of LH released into the medium during the second hour compared with the first hour of incubation. This priming effect of LHRH on LH secretion was accompanied by a significant margination of secretory granules and a drop in the total granule content of the gonadotrophs. Although the number of microfilaments remained the same, there was an increase in their length and a change in orientation so that the angle between the microfilaments and the plasmalemma was significantly reduced after both the first and second hour of exposure of LHRH. The addition of 14·3 μmol cytochalasin B/l to the incubation medium significantly increased the amount of LH released in the first hour of incubation when compared with the amount of LH released by LHRH alone, but completely abolished the priming effect of LHRH. Cytochalasin B also prevented the LHRH-induced increase in the length and the change in orientation of the microfilaments. These results indicate that LHRH priming involves an increase in length of microfilaments and a change in their orientation relative to the plasmalemma. J. Endocr. (1985) 106, 211–218

FEEDBACK EFFECT OF OESTROGEN ON LUTEINIZING HORMONE SECRETION BY THE RAT PITUITARY GLAND

1982 ◽  
Vol 92 (3) ◽  
pp. 389-395 ◽  
Author(s):  
TAKASHI HIGUCHI ◽  
MASAZUMI KAWAKAMI
Keyword(s):  
Pituitary Gland ◽  
Hormone Secretion ◽  
Feedback Effect ◽  
Ovariectomized Rats ◽  
Luteinizing Hormone Secretion ◽  
Hypothalamic Area ◽  
Serum Lh ◽  
Lh Rh ◽  
Lh Releasing Hormone ◽  
Lh Secretion

Ovariectomized rats with neural deafferentation at the level of the posterior border of the anterior hypothalamic area (AC rats) were used to re-evaluate the direct feedback effect of oestrogen on the regulation of LH secretion by the pituitary gland. Synthetic LH releasing hormone (LH-RH; 300 ng/kg), injected at 30-min intervals into AC rats with undetectable basal LH, induced pulsatile increase of serum LH concentrations. Oestradiol-17β (5 μg), administered i.v. just before the first LH-RH injection, significantly decreased the LH response to a second injection of LH-RH given 30 min later and to subsequent injections. Maximal inhibition was 58%. Oestradiol-17β (5 μg) given i.v. to control ovariectomized rats decreased serum LH concentrations 40 min after administration; the maximum reduction being 52%. An s.c. injection of oestradiol benzoate (5 μg) increased pituitary responsiveness to LH-RH by the next day in AC rats but decreased serum LH levels in control ovariectomized rats. These results indicate that acute inhibitory and chronic facilitatory effects of oestrogen on LH secretion are exerted at the pituitary gland, without a change in LH-RH secretion. The prolonged inhibitory effect of oestrogen is at the level of the hypothalamus and causes a reduction in LH-RH secretion.

The role of oestrogens on gonadotrophin secretion in the testicular feminization syndrome1

1980 ◽  
Vol 95 (3) ◽  
pp. 314-318 ◽  
Author(s):  
Martha Medina ◽  
Alfredo Ulloa-Aguirre ◽  
Maria A. Fernández ◽  
Gregorio Pérez-palacios
Keyword(s):  
Clomiphene Citrate ◽  
Poor Response ◽  
Testicular Feminization ◽  
Normal Response ◽  
Serum Lh ◽  
Gonadotrophin Secretion ◽  
Before And After ◽  
Complete Form ◽  
Lh Secretion

Abstract. The role of oestrogens on gonadotrophin secretion was assessed in three related patients with the complete form of testicular feminization syndrome. Serum LH and FSH levels were measured before and after I.RH stimulation as well as before, during and after chronic clomiphene citrate administration. Moderately elevated LH basal levels with a significant LH rise following I.RH were observed. Normal or even low FSH level with poor response to LRH were found in all subjects. Administration of clomiphene citrate resulted in a significant serum LH increase without any change of FSH. Following castration both LH and FSH rose and a normal response to LRH was observed. These results were interpreted as demonstrating that, while endogenous oestrogens modulate LH secretion in patients with androgen unresponsiveness, it plays no role in regulating FSH secretion and suggested that a factor of testicular origin without androgenic or oestrogenic activity is responsible for FSH regulation.

Effects of corticotropin-releasing hormone and its antagonist on the gene expression of gonadotrophin-releasing hormone (GnRH) and GnRH receptor in the hypothalamus and anterior pituitary gland of follicular phase ewes

2011 ◽  
Vol 23 (6) ◽  
pp. 780 ◽  
Author(s):  
Magdalena Ciechanowska ◽  
Magdalena Łapot ◽  
Tadeusz Malewski ◽  
Krystyna Mateusiak ◽  
Tomasz Misztal ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Follicular Phase ◽  
Gnrh Receptor ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion ◽  
Crh Receptors

There is no information in the literature regarding the effect of corticotropin-releasing hormone (CRH) on genes encoding gonadotrophin-releasing hormone (GnRH) and the GnRH receptor (GnRHR) in the hypothalamus or on GnRHR gene expression in the pituitary gland in vivo. Thus, the aim of the present study was to investigate, in follicular phase ewes, the effects of prolonged, intermittent infusion of small doses of CRH or its antagonist (α-helical CRH 9-41; CRH-A) into the third cerebral ventricle on GnRH mRNA and GnRHR mRNA levels in the hypothalamo–pituitary unit and on LH secretion. Stimulation or inhibition of CRH receptors significantly decreased or increased GnRH gene expression in the hypothalamus, respectively, and led to different responses in GnRHR gene expression in discrete hypothalamic areas. For example, CRH increased GnRHR gene expression in the preoptic area, but decreased it in the hypothalamus/stalk median eminence and in the anterior pituitary gland. In addition, CRH decreased LH secretion. Blockade of CRH receptors had the opposite effect on GnRHR gene expression. The results suggest that activation of CRH receptors in the hypothalamus of follicular phase ewes can modulate the biosynthesis and release of GnRH through complex changes in the expression of GnRH and GnRHR genes in the hypothalamo–anterior pituitary unit.

Adrenal progesterone facilitates the negative feedback of oestrogen on LH release in ovariectomized rats

1993 ◽  
Vol 139 (2) ◽  
pp. 253-258 ◽  
Author(s):  
A. M. Salicioni ◽  
R. W. Carón ◽  
R. P. Deis
Keyword(s):  
Ovariectomized Rats ◽  
Adrenal Steroids ◽  
Serum Progesterone ◽  
Oestrogen Treatment ◽  
Ovx Rats ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Lh Secretion

ABSTRACT There is evidence that the adrenals play a role in the regulation of the synthesis and release of gonadotrophins in various vertebrates. The aim of this study was to determine the part played by adrenal steroids, with special reference to progesterone, on the concentration of LH in ovariectomized (OVX) and oestrogen-primed rats. OVX rats received a single s.c. injection of vehicle or oestradiol benzoate (OB, 20 μg/rat). This day was designated as day 0. Three or four days later (day 3–day 4), the rats were treated with mifepristone (10 mg/kg) or with two doses of progesterone antiserum and blood samples were obtained at 13.00 and 18.00 h. OB treatment of OVX rats reduced serum LH at 13.00 h and 18.00 h on day 3 but only at 13.00 h on day 4. The administration of mifepristone at 08.00 h to OVX and oestrogen-treated rats induced a significant increase in serum LH at 18.00 h on days 3 and 4, without modifying the values at 13.00 h. When mifepristone was given at 13.00 h a much larger increase in serum LH was obtained at 18.00 h. In OVX and oestrogen-treated rats, adrenalectomy on day 2 (08.00–09.00 h) induced an increase in serum LH at 18.00 h similar to that observed in the OVX and oestrogen-primed rats after mifepristone treatment. In order to determine the specificity of the effect of mifepristone, a group of OVX and oestrogentreated rats was injected with progesterone antiserum at 08.00 and 13.00 h on day 3. Serum LH concentrations at 13.00 and 18.00 h on day 3 were similar to values obtained in OVX rats treated with oestrogen and mifepristone. Serum progesterone was measured at 08.00 and 13.00 h in OVX and OVX and oestrogenprimed rats. At both times, values were similar in OVX rats but oestrogen treatment significantly increased serum progesterone levels. The important role of adrenal progesterone on the regulation of LH secretion in OVX and oestrogen-primed rats is evident from these results. Blocking progesterone action at the receptor level, we showed that OB significantly increased LH values at 18.00 h. On the basis of these studies it is tempting to speculate on the possibility of an inhibitory or stimulatory effect of oestrogen on serum LH concentration in OVX rats, according to the presence or absence of adrenal progesterone action. Journal of Endocrinology (1993) 139, 253–258

Changes in pituitary responsiveness to LH-releasing hormone after acute buserelin treatment: a time-course and dose–response study

1985 ◽  
Vol 106 (1) ◽  
pp. 27-30 ◽  
Author(s):  
J. D. Heather ◽  
S. A. Whitehead
Keyword(s):  
Time Course ◽  
Dependent Manner ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Significant Difference ◽  
Lh Release ◽  
Lh Releasing Hormone ◽  
In Vivo Effects ◽  
Dose Response Study

ABSTRACT The acute in-vivo effects of a potent LH-releasing hormone (LHRH) agonist, buserelin, on LH secretion and pituitary responsiveness to LHRH have been investigated in oestrous rats. Doses of 50, 100 and 250 ng buserelin stimulated LH release in a dose-dependent manner, the peak serum LH concentrations being measured 1 h after the treatment. Thereafter LH levels fell rapidly between 1 and 6 h and by 18 h serum LH concentrations were similar in all groups of animals. Pituitary responsiveness to a challenge with 100 ng LHRH was potentiated by 50 or 100 ng buserelin injected 1 or 2 h before the LHRH challenge. In contrast, 250 ng buserelin completely abolished the LH response to LHRH when tested 1, 2 and 4 h after treatment, but by 6 h a small but attenuated response was observed. Four hours after treatment there was no significant difference in the responses when compared with the saline-treated controls. J. Endocr. (1985) 106, 27–30

scholarly journals Effects of treatment with LH releasing hormone before the early increase in LH secretion on endocrine and reproductive development in bull calves

Reproduction ◽  
1997 ◽  
Vol 111 (1) ◽  
pp. 41-50 ◽  
Author(s):  
R. K. Chandolia ◽  
A. Honaramooz ◽  
P. M. Bartlewski ◽  
A. P. Beard ◽  
N. C. Rawlings
Keyword(s):  
Reproductive Development ◽  
Releasing Hormone ◽  
Bull Calves ◽  
Early Increase ◽  
Lh Releasing Hormone ◽  
Lh Secretion

Pituitary and testicular responses in sexually mature bulls after intravenous injections of graded doses of LH-releasing hormone

1984 ◽  
Vol 103 (3) ◽  
pp. 371-376 ◽  
Author(s):  
M. J. D'Occhio ◽  
B. P. Setchell
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Anterior Pituitary Gland ◽  
Limiting Factor ◽  
Releasing Hormone ◽  
Intravenous Injections ◽  
Gonadotrophin Secretion ◽  
Lh Release ◽  
Lh Releasing Hormone ◽  
Sexually Mature

ABSTRACT The capacity of the anterior pituitary gland and testes in mature bulls (705±9 (s.e.m.) kg body wt, n = 4) to respond to graded doses of LH-releasing hormone (LHRH) was assessed relative to endogenous profiles of LH and testosterone secretion. Endogenous hormone profiles were determined by bleeding bulls at 20-min intervals for 12 h. Responses to LHRH were assessed on successive days after single intravenous injections of 1, 5, 10, 50 or 100 ng LHRH/kg body wt. Blood samples were taken at −40, −20, 0, 10, 20, 30, 40, 60 and 120 min relative to LHRH injection. During a 12-h bleed bulls showed spontaneous pulses of LH and testosterone which had peak amplitudes of 2·6±0·5 μg/l and 44·5 ± 7·1 nmol/l respectively. Respective peak LH (μg/l) and testosterone (nmol/l) responses to LVRH were as follows: 1 ng LHRH (3·0±0·7: 47·3±4·1); 5 ng LHRH (8·0±1·2; 52·8 ± 6·2); 10 ng LHRH (11·1±2·3; 57·7 ± 9·1); 50 ng LHRH (19·2±2·8; 47·9±8·6); 100 ng LHRH (19·1±4·7; 43·9 ±6·4). A dose of 1 ng LHRH/kg produced LH and testosterone responses which were comparable in amplitude to spontaneous peaks in the respective hormone. There was a linear (y = 0·28x+5·72; r = 0·81) increase in the LH response to doses of LVRH between 1 and 50 ng/kg; corresponding testosterone responses showed no relationship with the dose of LHRH. The capacity of the anterior pituitary gland to release amounts of LH eight to ten times in excess of those secreted during spontaneous peaks suggests that (1) there exists a large releasable store of LH in the anterior pituitary gland and (2) hypothalamic LHRH is a limiting factor in gonadotrophin secretion. In contrast to LH release, the androgenic response of the testes to acute gonadotrophic stimulation is determined largely by prevailing steroidogenic activity. J. Endocr. (1984) 103, 371–376

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