scholarly journals Stimulation of LH secretion in sheep by central administration of corticotrophin-releasing hormone

Reproduction ◽  
1997 ◽  
Vol 111 (2) ◽  
pp. 249-257 ◽  
Author(s):  
A. Caraty ◽  
D. W. Miller ◽  
B. Delaleu ◽  
G. B. Martin
Keyword(s):  
Central Administration ◽  
Releasing Hormone ◽  
Lh Secretion ◽  
Stimulation Of

Brain oxytocin receptors mediate corticotropin-releasing hormone-induced anorexia

1991 ◽  
Vol 260 (2) ◽  
pp. R448-R452 ◽  
Author(s):  
B. R. Olson ◽  
M. D. Drutarosky ◽  
E. M. Stricker ◽  
J. G. Verbalis
Keyword(s):  
Food Intake ◽  
Adrenocorticotropic Hormone ◽  
Central Administration ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Oxytocin Receptors ◽  
Artificial Cerebrospinal Fluid ◽  
Pituitary Secretion ◽  
Inhibit Food Intake ◽  
Stimulation Of

Central administration of corticotropin-releasing hormone (CRH) is known to inhibit food intake and stimulate pituitary oxytocin (OT) secretion in rats. These experiments addressed the possibility that the inhibition of food intake that follows central CRH administration is mediated through oxytocinergic pathways. Male food-deprived rats, with stable baseline food intakes after intracerebroventricular (icv) injections of artificial cerebrospinal fluid, received 150 pmol of CRH icv. Food intake was inhibited by 62 +/- 5% during a 90-min test period. Pretreatment with 9 nmol of the OT antagonist [d(CH2)5, Tyr(Me)2, Orn8]vasotocin icv completely eliminated the inhibition of food intake produced by icv CRH. In contrast, pretreatment with the OT-receptor antagonist did not significantly alter pituitary secretion of adrenocorticotropic hormone and OT stimulated by icv CRH. The results of these experiments implicate OT as a possible central mediator of CRH-induced anorexias in rats, particularly those that are accompanied by stimulation of neurohypophysial OT secretion.

Stimulation of corticotropin-releasing hormone-mediated adrenocorticotropin secretion by central administration of prolactin-releasing peptide in rats

2000 ◽  
Vol 285 (3) ◽  
pp. 234-238 ◽  
Author(s):  
Hirokazu Matsumoto ◽  
Minoru Maruyama ◽  
Jiro Noguchi ◽  
Yasuko Horikoshi ◽  
Ken Fujiwara ◽  
...  
Keyword(s):  
Central Administration ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Prolactin Releasing Peptide ◽  
Stimulation Of

Circulating gonadotrophin surge-attenuating factor from superovulated women suppresses in vitro gonadotrophin-releasing hormone self-priming

1994 ◽  
Vol 143 (1) ◽  
pp. 45-54 ◽  
Author(s):  
P A Fowler ◽  
P Cunningham ◽  
M Fraser ◽  
F MacGregor ◽  
B Byrne ◽  
...  
Keyword(s):  
Follicular Fluid ◽  
Peripheral Circulation ◽  
Basal Secretion ◽  
Releasing Hormone ◽  
Significant Difference ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion ◽  
Marked Suppression ◽  
Stimulation Of

Abstract A penfusion system based on ovine pituitary tissue explants was used to investigate the effects of follicular fluid (hFF) and serum from superovulated women on pituitary responsiveness to gonadotrophin-releasing hormone (GnRH). The specific aims of the study were to determine both if gonadotrophin surge-attenuating factor (GnSAF) bioactivity is present in the peripheral circulation as well as in the follicles of superovulated women and if GnSAF suppresses GnRH self-priming in vitro. Two pulses of GnRH, 1 h apart, produced marked peaks in LH secreted from control chambers, with GnRH self-priming evident in the significant difference between the first (134·4±1·7–232·1±24·0% of basal secretion) and second (183·9±15·8–313·9±14·0% of basal secretion) LH peaks. Both follicular fluid and serum pooled from two different groups of women produced marked suppression of the first (unprimed) and second (primed) LH peaks. The hFF reduced the first LH peak to 69·6±7·8 and 60·2±9·7% and the second LH peak to 57·4±6·7 and 42·6±6·5% of control LH secretion. Overall, the serum reduced the first and second LH peaks to 76·8±4·2 and 62·9±3·6% of control respectively. These results demonstrated that GnSAF bioactivity suppresses GnRH self-priming, and is present in both the peripheral circulation and hFF. The same material administered to dispersed ovine pituitary monolayers produced similar marked suppression of GnRH-induced LH secretion, with approximately 50-fold less GnSAF bioactivity in serum compared with hFF. Combined doses of oestradiol and progesterone, or hFF from large follicles containing little GnSAF, produced stimulation of GnRH-induced LH secretion and GnRH self-priming (second peaks 78·1±38·9 and 27·4±15·7% respectively higher than first peaks). Thus, in conclusion, GnSAF in hFF and serum markedly attenuated both unprimed and primed pituitary response to GnRH, virtually abolishing the GnRH self-priming effect. Journal of Endocrinology (1994) 143, 45–54

EFFECT OF GONADAL STEROIDS ON THE PITUITARY RESPONSIVENESS TO SYNTHETIC LUTEINIZING HORMONE RELEASING HORMONE IN THE MALE DOG

1974 ◽  
Vol 61 (1) ◽  
pp. 123-131 ◽  
Author(s):  
GWYNETH E. JONES ◽  
A. R. BOYNS
Keyword(s):  
Luteinizing Hormone ◽  
Gonadal Steroids ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Intravenous Injections ◽  
Lh Rh ◽  
Lh Secretion ◽  
Stimulation Of

SUMMARY Intravenous injections of synthetic luteinizing hormone releasing hormone (LH-RH) stimulated LH secretion in male dogs. An i.m. injection of 0·025–2·5 mg oestradiol-17β given 2·5 h but not 24 h before administration of LH-RH blocked LH secretion. Diethylstilboestrol (2·5 mg) also blocked LH secretion but meso-dihydrodibutylstilboestrol (2·5 mg) was without effect. Testosterone (2·5 and 25 mg), dihydrotestosterone (2·5 mg), 5α-androstane-3α, 17β-diol (2·5 mg), 5α-androstane-3β, 17β-diol (2·5 mg), 5α-androstane-3α, 17α-diol (0·125 mg), 5α-androstane-3β, 17α-diol (0·125 mg) and progesterone (25 and 50 mg) did not prevent LH-RH stimulation of LH secretion.

Central administration of corticotrophin-releasing factor in the sheep: effects on secretion of gonadotrophins, prolactin and cortisol

1990 ◽  
Vol 124 (1) ◽  
pp. 117-125 ◽  
Author(s):  
A. M. Naylor ◽  
D. W. F. Porter ◽  
D. W. Lincoln
Keyword(s):  
Pituitary Gland ◽  
Opioid Peptides ◽  
Anterior Pituitary ◽  
Anterior Pituitary Gland ◽  
Central Administration ◽  
Endogenous Opioid Peptides ◽  
Endogenous Opioid ◽  
Corticotrophin Releasing Factor ◽  
Lh Secretion ◽  
Stimulation Of

ABSTRACT Stress interferes with the normal secretion of LH and FSH from the anterior pituitary gland and therefore exerts a deleterious effect on reproductive function. Evidence suggests that the stress-induced disruption of gonadal function is due to a central action of corticotrophin-releasing factor (CRF) to inhibit the release of LHRH into the hypophysial-portal circulation. The following studies were undertaken to investigate further the role of CRF in regulating gonadotrophin release in the sheep and to determine whether central administration of this peptide can alter the secretion of other hormones (e.g. prolactin and cortisol) known to be released under conditions of stress. In contrast to other species, injection of CRF into the third ventricle of the sheep brain caused a dose-related stimulation of LH secretion. The pulse frequency and mean levels of LH were increased significantly following central administration of CRF. In contrast to this effect, central administration of CRF did not alter the plasma concentration of FSH but caused a marked and dose-related stimulation of prolactin and cortisol secretion. The stimulatory effect of CRF on prolactin secretion was reversed by i.v. administration of the opioid antagonist naloxone, suggesting that endogenous opioid peptides mediate the central effect of CRF on the release of prolactin, but not cortisol. In conclusion, these data demonstrate that administration of CRF causes a dose-related stimulation of LH and prolactin release from the anterior pituitary gland and cortisol from the adrenal gland. In the case of prolactin, endogenous opioid peptides are likely to mediate this response. The observations concerning LH are the opposite of those reported for the rat and the monkey where CRF caused a prolonged inhibition of gonadotrophin secretion. This suggests that a species difference may exist or, alternatively, the stimulatory effect of CRF on LH secretion in the sheep may be similar to the increase in LH secretion reported in rats and monkeys subjected to short-term handling or restraint stress. Journal of Endocrinology (1990) 124, 117–125

scholarly journals Central administration of corticotrophin releasing hormone but not arginine vasopressin stimulates the secretion of luteinizing hormone in rams in the presence and absence of testosterone

1999 ◽  
Vol 162 (2) ◽  
pp. 301-311 ◽  
Author(s):  
AJ Tilbrook ◽  
BJ Canny ◽  
BJ Stewart ◽  
MD Serapiglia ◽  
IJ Clarke
Keyword(s):  
Arginine Vasopressin ◽  
Testosterone Propionate ◽  
Plasma Concentrations ◽  
Pulse Amplitude ◽  
Central Administration ◽  
Releasing Hormone ◽  
Adrenal Steroid ◽  
Reproductive Axis ◽  
Cortisol Levels ◽  
Lh Secretion

This study tested the hypothesis that central administration of corticotrophin-releasing hormone (CRH) and/or arginine vasopressin (AVP) will affect the secretion of LH in rams and that testosterone is necessary for these actions to occur. Plasma LH levels were measured in castrated rams during 1 h infusion of either 100 microliter vehicle/mock cerebrospinal fluid (CSF) or mock CSF containing 25 microgram CRH, 25 microgram AVP or 25 microgram of each peptide through guide cannulae into the third cerebral ventricle. These intracerebroventricular (i.c.v.) infusions were given to the castrated rams following injections (i.m.) each 12 h of oil or 8 mg testosterone propionate for 7 days. Blood samples were collected every 10 min for 4 h before i.c.v. infusion, during infusion and for 4 h following the infusion. Infusion of vehicle did not affect any endocrine parameters. In contrast, the plasma concentrations of LH and the amplitude of LH pulses were increased significantly during and following infusion of CRH, and this effect was not influenced by whether the castrated rams were treated with testosterone propionate or whether the CRH was administered in combination with AVP. Infusion of AVP alone did not affect LH secretion. The frequency of LH pulses and the plasma concentrations of FSH did not change with any of the i.c.v. treatments. The plasma concentrations of cortisol were significantly increased by CRH and AVP infusions. The plasma concentrations of cortisol achieved during and following i.c.v. infusion of CRH and AVP combined were greater than the concentrations achieved as a result of treatment with AVP alone but were similar to those with CRH. There was no effect of testosterone propionate on cortisol levels. These results show that CRH, but not AVP, is capable of acting either centrally or at the pituitary level to increase the secretion of LH in rams and these actions are not affected by testosterone. The stimulatory effects of CRH on LH secretion are to increase the amplitude of GnRH pulses and/or the responsiveness of the pituitary to the actions of GnRH with no effect on the frequency of GnRH pulses. The secretion of FSH in rams is not influenced by either CRH or AVP. The effect of CRH to increase LH pulse amplitude occurs in the face of increased cortisol levels, further reinforcing our belief that this adrenal steroid does not affect the reproductive axis in this species.

scholarly journals Stimulation of Gonadotropin-Releasing Hormone Surges by Estrogen. II. Role of Cyclic Adenosine 3′,5′-Monophosphate

Endocrinology ◽  
2000 ◽  
Vol 141 (4) ◽  
pp. 1486-1492 ◽  
Author(s):  
Patrick E. Chappell ◽  
Juliet Lee ◽  
Jon E. Levine
Keyword(s):  
Gonadotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Stimulation Of
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