Suppression of LH response to gonadotrophin-releasing hormone or oestradiol by ACTH(1–24) treatment in anoestrous ewes

1988 ◽  
Vol 118 (2) ◽  
pp. 193-197 ◽  
Author(s):  
H. Dobson ◽  
S. A. Essawy ◽  
M. G. S. Alam
Keyword(s):  
Plasma Concentrations ◽  
Suppressive Effect ◽  
Reproductive Efficiency ◽  
Adrenocorticotrophic Hormone ◽  
Releasing Hormone ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Baseline Values ◽  
Lh Secretion

ABSTRACT Stress is known to result in lowered female reproductive efficiency. The objective of this study was to examine how increased pituitary-adrenal activity may influence gonadotrophin release in anoestrous ewes. Various doses (0·06–1·0 mg) of a synthetic adrenocorticotrophic hormone (ACTH(1–24)) preparation were injected into ewes 30 min or 3 h before an i.v. injection of 500 ng gonadotrophin-releasing hormone (GnRH). The LH response to GnRH given 30 min after ACTH(1–24) was similar to that after GnRH alone, whereas the response 3 h after ACTH(1–24) was significantly lower, irrespective of the dose of ACTH(1–24). At 30 min and 3 h after ACTH(1–24) the concentrations of cortisol exceeded 50 nmol/l compared with baseline values of < 10 nmol/l. The effect of ACTH(1–24) on oestradiol-induced LH release was also examined. Those ewes receiving 0·8 mg ACTH(1–24) depot and 50 μg oestradiol benzoate simultaneously had a preovulatory-type increase in LH 14–20 h later, similar to when oestradiol benzoate was given alone. None of the ewes receiving an additional 0·8 mg ACTH(1–24) depot 10 h after oestradiol benzoate had increases in LH concentration. The cortisol concentrations in all ewes receiving either one or two injections of ACTH(1–24) were > 35 nmol/l at 10 h after the oestradiol injection. However, concentrations of progesterone increased from 0·9 ± 0·3 (s.e.m.) nmol/l at the time of the second ACTH(1–24) injection to 2·1 ±0·3 nmol/l after 2 h. In summary, it would appear that the suppressive effect of ACTH(1–24) on LH secretion induced by GnRH or oestradiol in the anoestrous ewe is not dependent on increased plasma concentrations of cortisol. J. Endocr. (1988) 118, 193–197

Pulsatile administration of gonadotrophin-releasing hormone stimulates, in oestrogen-treated anaesthetized ovariectomized ewes, a surge release of LH qualitatively and quantitatively different from that induced by oestradiol in conscious ovariectomized ewes

1988 ◽  
Vol 116 (1) ◽  
pp. 143-148 ◽  
Author(s):  
P. J. Wright ◽  
I. J. Clarke
Keyword(s):  
Plasma Concentrations ◽  
Lh Surge ◽  
Releasing Hormone ◽  
Treatment Regimens ◽  
Oestradiol Benzoate ◽  
Pulsatile Administration ◽  
Gonadotrophin Releasing Hormone ◽  
Induction Of Anaesthesia ◽  
Lh Secretion ◽  
Conscious Control

ABSTRACT The nature of the gonadotrophin-releasing hormone (GnRH) stimulus of the pituitary necessary for the oestrogen-induced plasma LH surge was studied in ovariectomized ewes. The sheep were treated with oestradiol benzoate (50 μg i.m.) at 0 h, and the hypothalamic contribution to the LH surge was blocked by pentobarbitone anaesthesia over the time during which the surge was expected (11–31 h). Pituitary responsiveness to exogenous GnRH (100 ng) administered i.v. in a pulsatile mode (once per hour or once per 20 min) over the period 15–30 h was assessed from plasma concentrations of LH. Neither of the GnRH treatments induced patterns of LH secretion similar to those seen in conscious ovariectomized ewes given oestrogen only. Plasma LH secretion in response to hourly GnRH pulses was less (P<0·01) than that associated with oestrogen-induced plasma LH surges in conscious control ewes. With pulses of GnRH administered every 20 min the amount of LH released was greater (P<0·05) than that in oestrogen-treated conscious control ewes. In contrast to the single surge induced by oestradiol in conscious ewes, GnRH pulses given every 20 min elicited phasic patterns of LH secretion consisting of two or three distinct surges. The failure of GnRH treatment to elicit an LH surge similar to an oestrogen-induced surge could reflect inappropriate GnRH treatment regimens, and/or inadequate priming of the pituitary with GnRH after induction of anaesthesia but before GnRH treatment. J. Endocr. (1988) 116, 143–148

Infantile ovariectomy potentiates the stimulatory effect of oestrogen/progesterone on LH secretion in the rat

1985 ◽  
Vol 106 (1) ◽  
pp. 133-139 ◽  
Author(s):  
M. Wilkinson ◽  
R. Bhanot
Keyword(s):  
Inhibitory Mechanism ◽  
Releasing Hormone ◽  
Oestradiol Benzoate ◽  
Gonadotrophin Releasing Hormone ◽  
Prepubertal Rats ◽  
Lh Secretion

ABSTRACT Ovariectomy of prepubertal rats (9 days of age) eliminates the ability of the opiate peptide FK 33-824 to inhibit LH secretion when tested 19 days later. We have investigated whether this removal of opiate inhibition would modify the LH/FSH response to stimulation with oestradiol benzoate/progesterone priming. Ovariectomy of rats during infancy (9 days after birth) amplifies the stimulatory effects of these steroids on LH/FSH secretion when tested 19 days later. This amplification was not seen in rats ovariectomized before (day 24) or after puberty (day 43) and tested 19 days later. The pituitary content of LH/FSH does not appear to contribute to this phenomenon, though increased responsiveness to injected gonadotrophin-releasing hormone (GnRH) is clearly involved; ovariectomy at day 9 is considerably more effective than ovariectomy at day 24 of life in enhancing the response to GnRH. We conclude that infantile ovariectomy either removes, or prevents the development of, a hypothalamic inhibitory mechanism which normally modulates the responsiveness of the pituitary to stimulation with GnRH. J. Endocr. (1985) 106, 133–139

Effects of crude and highly purified bovine inhibin (Mr 32 000 form) on gonadotrophin production by ovine pituitary cells in vitro: inhibin enhances gonadotrophin-releasing hormone-induced release of LH

1990 ◽  
Vol 127 (1) ◽  
pp. 149-159 ◽  
Author(s):  
S. Muttukrishna ◽  
P. G. Knight
Keyword(s):  
Primary Cultures ◽  
Suppressive Effect ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
Α Subunit ◽  
Releasing Hormone ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone

ABSTRACT Primary cultures of ovine pituitary cells (from adult ewes) were used to investigate the actions of steroid-free bovine follicular fluid (bFF) and highly-purified Mr 32 000 bovine inhibin on basal and gonadotrophin-releasing hormone (GnRH)-induced release of FSH and LH. Residual cellular contents of each hormone were also determined allowing total gonadotrophin content/well to be calculated. As in rats, both crude and highly purified inhibin preparations promoted a dose (P < 0·001)- and time (P < 0·001)-dependent suppression of basal and GnRH-induced release of FSH as well as an inhibition of FSH synthesis, reflected by a fall in total FSH content/well. However, while neither inhibin preparation affected basal release of LH or total LH content/well, GnRH-induced LH release was significantly (P< 0·001) increased by the presence of either bFF (+ 75%) or highly-purified inhibin (+ 64%) in a dose- and time-dependent manner. This unexpected action of bFF on GnRH-induced LH release was abolished in the presence of 5 μl specific anti-inhibin serum, confirming that the response was indeed mediated by inhibin. Furthermore, neither oestradiol-17β (1 pmol/l–10 nmol/l) nor monomeric α-subunit of bovine inhibin (2·5–40 ng/ml) significantly affected basal or GnRH-induced release of LH. These in-vitro findings for the ewe lend support to a number of recent in-vivo observations and indicate that, in addition to its well-documented suppressive effect on the synthesis and secretion of FSH, inhibin may actually facilitate LH release in this species, in marked contrast to its action in the rat. Journal of Endocrinology (1990) 127, 149–159

The oestrogen-induced surge of LH requires a 'signal' pattern of gonadotrophin-releasing hormone input to the pituitary gland in the ewe

1989 ◽  
Vol 122 (1) ◽  
pp. 127-134 ◽  
Author(s):  
I. J. Clarke ◽  
J. T. Cummins ◽  
M. Jenkin ◽  
D. J. Phillips
Keyword(s):  
Pituitary Gland ◽  
Pulse Amplitude ◽  
Pulse Frequency ◽  
Lh Surge ◽  
Releasing Hormone ◽  
Gnrh Secretion ◽  
Signal Pattern ◽  
Oestradiol Benzoate ◽  
Gonadotrophin Releasing Hormone ◽  
Baseline Values

ABSTRACT Two experiments were conducted with ovariectomized and hypothalamo-pituitary disconnected (HPD) ewes to ascertain the pattern of inputs, to the pituitary gland, of gonadotrophin-releasing hormone (GnRH) necessary for the full expression of an oestrogen-induced LH surge. The standard GnRH replacement to these sheep was to give pulses of 250 ng (i.v.) every 2 h; at the onset of experimentation, pulses were given hourly. In experiment 1, groups of sheep (n = 7) were given an i.m. injection of 50 μg oestradiol benzoate, and after 10 h the GnRH pulse frequency or pulse amplitude was doubled. Monitoring of plasma LH concentrations showed that a doubling of pulse frequency produced a marked increase in baseline values, whereas a doubling of amplitude had little effect on the LH response. In a second experiment, ovariectomized HPD sheep that had received hourly pulses of GnRH for 16 h after an i.m. injection of oil or 50 μg oestradiol benzoate were given either a 'bolus' (2·25 μg GnRH) or a 'volley' (500 ng GnRH pulses 10 min apart for 30 min, plus a 500 ng pulse 15 min later). Both groups then received GnRH pulses (250 ng) every 30 min for the next 13 h. Oestrogen enhanced the LH responses to the GnRH treatments, and the amount of LH released was similar in ovariectomized HPD ewes given oestrogen plus bolus or volley GnRH treatments and ovariectomized hypothalamopituitary intact ewes given oestrogen. These results suggest that the oestrogen-induced LH surge is initiated by a 'signal' pattern of GnRH secretion from the hypothalamus. Journal of Endocrinology (1989) 122, 127–134

Differential responses of hypothalamic LHRH-I and -II to castration and gonadal steroid or tamoxifen treatment in cockerels

1990 ◽  
Vol 125 (1) ◽  
pp. 139-146 ◽  
Author(s):  
S. C. Wilson ◽  
R. T. Gladwell ◽  
F. J. Cunningham
Keyword(s):  
Plasma Concentration ◽  
Testosterone Propionate ◽  
Plasma Concentrations ◽  
Suppressive Effect ◽  
Posterior Hypothalamus ◽  
Gonadal Steroids ◽  
Tamoxifen Treatment ◽  
Gonadal Steroid ◽  
Oestradiol Benzoate ◽  
Lh Secretion

ABSTRACT Changes in the hypothalamic contents of LHRH-I and LHRH-II were determined in intact and castrated cockerels injected i.m. with gonadal steroids or tamoxifen. An increase in the plasma concentration of LH after castration was accompanied by a significant increase in the content of LHRH-I in the posterior hypothalamus (including the mediobasal hypothalamus and median eminence) which was reversed by oestradiol benzoate given on days 14 and 15 after castration. Under similar circumstances, testosterone propionate did not modify the hypothalamic content of LHRH-I, even though both steroids reduced the plasma concentrations of LH to levels below those of intact cockerels. Treatment of intact cockerels with oestradiol benzoate significantly increased the content of LHRH-I in the posterior hypothalamus, whilst testosterone propionate was again without effect. Tamoxifen significantly raised the plasma concentration of LH in intact cockerels and partially antagonized the suppressive effect of oestradiol benzoate and testosterone on LH secretion in castrated cockerels. However, an anti-oestrogenic effect of tamoxifen on the hypothalamic content of LHRH-I was not demonstrated. There was no evidence of any changes in the hypothalamic content of LHRH-II after castration, with or without gonadal steroid replacement. A change in the hypothalamic content of LHRH-I in response to manipulation of the steroid environment would imply an involvement of this peptide in the mechanism by which gonadal steroids regulate the release of LH. The absence of changes in the hypothalamic content of LHRH-II in the same circumstances suggest that it is not directly involved in the control of LH secretion by the gonadal steroid negative feedback loop. Journal of Endocrinology (1990) 125, 139–146

Effect of stress during shearing on the LH response to GnRH in anoestrous ewes

1988 ◽  
Vol 110 (3) ◽  
pp. 673-676 ◽  
Author(s):  
Hilary Dobson
Keyword(s):  
Luteinizing Hormone ◽  
Present Experiment ◽  
Plasma Cortisol ◽  
Reproductive Efficiency ◽  
Environmental Stressor ◽  
Considerable Evidence ◽  
Releasing Hormone ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Cortisol Release

There is considerable evidence that stress causes an increase in plasma cortisol concentrations in sheep (Stephens, 1980). Stress had deleterious effects on female reproductive efficiency (Christian, Lloyd & Davies, 1965) possibly, in part, by suppression of gonadotrophin release by increased pituitaryadrenal activity (Wagner & Li, 1982; Moberg, 1984). Previous experiments from our laboratory (Dobson, Essawy & Alam, 1988) have shown that administration of synthetic adrenocorticotrophin hormone (ACTH 1–24) results both in increased cortisol release and suppression of the luteinizing hormone (LH) response to gonadotrophin releasing hormone (GnRH). The purpose of the present experiment was to investigate whether LH release is suppressed in ewes subjected to an environmental stressor.

Interaction between cortisol and arachidonic acid on the secretion of LH from ovine pituitary tissue

1991 ◽  
Vol 131 (1) ◽  
pp. 87-94 ◽  
Author(s):  
A. W. Nangalama ◽  
G. P. Moberg
Keyword(s):  
Arachidonic Acid ◽  
Plasma Membrane ◽  
Suppressive Effect ◽  
Inhibitory Effect ◽  
Adrenal Steroids ◽  
Membrane Phospholipids ◽  
Pituitary Tissue ◽  
Receptor Sites ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone

ABSTRACT In several species, glucocorticoids act directly on the pituitary gonadotroph to suppress the gonadotrophin-releasing hormone (GnRH)-induced secretion of the gonadotrophins, especially LH. A mechanism for this action of these adrenal steroids has not been established, but it appears that the glucocorticoids influence LH release by acting on one or more post-receptor sites. This study investigated whether glucocorticoids disrupt GnRH-induced LH release by altering the liberation of arachidonic acid from plasma membrane phospholipids, a component of GnRH-induced LH release. Using perifused ovine pituitary tissue, it was established that exposure of gonadotrophs to 1–1000 nmol cortisol/l for 4 h or longer significantly reduced GnRH-stimulated LH release with the maximal inhibitory effect being observed after 6 h of exposure to cortisol. This suppressive effect of cortisol could be reversed by administration of arachidonic acid, which in its own right could stimulate LH release from ovine pituitary tissue. Furthermore, the inhibitory effect of cortisol on GnRH-stimulated LH release could be directly correlated with decreased pituitary responsiveness to GnRH-stimulated arachidonic acid liberation, consistent with our hypothesis that glucocorticoids can suppress GnRH-induced secretion of LH by reducing the amount of arachidonic acid available for the exocytotic response of GnRH. Journal of Endocrinology (1991) 131, 87–94

Plasma LH and testosterone responses to gonadotrophin-releasing hormone in adult red deer (Cervus elaphus) stags during the annual antler cycle

1988 ◽  
Vol 117 (1) ◽  
pp. 35-41 ◽  
Author(s):  
P. F. Fennessy ◽  
J. M. Suttie ◽  
S. F. Crosbie ◽  
I. D. Corson ◽  
H. J. Elgar ◽  
...  
Keyword(s):  
Red Deer ◽  
Plasma Concentrations ◽  
Reproductive Hormones ◽  
Sexual Cycle ◽  
Late Winter ◽  
Releasing Hormone ◽  
Antler Growth ◽  
Velvet Antler ◽  
Antler Cycle ◽  
Gonadotrophin Releasing Hormone

ABSTRACT Eight adult red deer stags were given an i.v. injection of synthetic gonadotrophin-releasing hormone (GnRH) on seven occasions at various stages of the antler cycle, namely hard antler in late winter, casting, mid-velvet growth, full velvet growth, antler cleaning and hard antler both during the rut and in mid-winter. The stags were allocated at random on each occasion to one of four doses, i.e. 1, 3, 10 or 95 μg GnRH. Blood samples were taken before GnRH injection and for up to 2 h after injection. Pituitary and testicular responses were recorded in terms of plasma LH and testosterone concentrations. There was an increase in plasma concentration of LH after the GnRH injection in all stags at all stages of the antler cycle. Dose-dependent responses of LH to GnRH in terms of area under the curve were apparent at all stages of the antler cycle. The lowest responses were recorded at casting, during velvet antler growth and at the rut sampling. The pattern of testosterone response reflected the inter-relationship of the antler and sexual cycles with very low testosterone responses occurring at casting and during velvet antler growth. The responses were higher at antler cleaning and then increased to a maximum at the rut before declining to reach their nadir at casting. The results are consistent with a hypothesis that the antler cycle, as a male secondary sexual characteristic, is closely linked to the sexual cycle and its timing is controlled by reproductive hormones. Low plasma concentrations of testosterone, even after LH stimulation, are consistent with the hypothesis that testosterone is unnecessary as an antler growth stimulant during growth. J. Endocr. (1988) 117, 35–41

Modulatory effect of steroid hormones on GnRH-induced LH secretion by cultured rat pituitary cells

1992 ◽  
Vol 70 (7) ◽  
pp. 963-969 ◽  
Author(s):  
Gabriela T. Pérez ◽  
Marta E. Apfelbaum
Keyword(s):  
Steroid Hormones ◽  
Pituitary Cells ◽  
Short Term ◽  
Stimulatory Action ◽  
Rat Pituitary ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Rat Pituitary Cells ◽  
Lh Secretion

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.

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