ACUTE EFFECTS OF HYPOTHALAMIC LESIONS UPON GONADOTROPHIN SECRETION IN THE FERRET

1981 ◽  
Vol 89 (3) ◽  
pp. 329-336 ◽  
Author(s):  
B. T. DONOVAN ◽  
M. B. TER HAAR
Keyword(s):  
Platinum Electrodes ◽  
Acute Effects ◽  
Hypothalamic Lesions ◽  
Gonadotrophin Secretion ◽  
Lh Release ◽  
High Concentrations ◽  
Lh Secretion ◽  
Steel Electrodes

The changes in FSH and LH secretion after placement of lesions in the hypothalamus were traced in ferrets serially bled at 15 min intervals. Passage of the lesioning current through platinum electrodes in anoestrous females was associated with an immediate surge in LH and FSH output. Damage to the hypothalamus of oestrous females also caused an immediate surge of LH secretion, but then a long-lasting second rise in blood LH content set in. High concentrations of LH were never sustained overnight. The response of long-term spayed females to the placement of hypothalamic lesions was similar to that of anoestrous ferrets, while that of anoestrous or oestrous ferrets was not altered by acute removal of the ovaries. Manipulation of the ovaries appeared to facilitate FSH and LH secretion. The response of males was similar to that of anoestrous females. Marked increases in FSH and LH release were also seen in females when lesions were made with steel electrodes, but had subsided on the following day.

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.

Influence of melatonin and oestradiol on the opioidergic regulation of LH and prolactin release in pony mares

1997 ◽  
Vol 154 (2) ◽  
pp. 241-248 ◽  
Author(s):  
C Aurich ◽  
J Lange ◽  
H-O Hoppen ◽  
J E Aurich
Keyword(s):  
Prolactin Secretion ◽  
Opioid Antagonist ◽  
Short Term ◽  
Melatonin Treatment ◽  
Prolactin Release ◽  
Oestradiol Treatment ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Lh Secretion

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

The inhibitory effect of opiates on gonadotrophin secretion is dependent upon gonadal steroids

1984 ◽  
Vol 102 (2) ◽  
pp. 133-141 ◽  
Author(s):  
R. Bhanot ◽  
M. Wilkinson
Keyword(s):  
Negative Feedback ◽  
Prolactin Secretion ◽  
Gonadal Steroids ◽  
Female Rats ◽  
Inhibitory Effects ◽  
Endogenous Opiates ◽  
Gonadotrophin Secretion ◽  
Oestradiol Benzoate ◽  
Lh Secretion

ABSTRACT We have attempted to clarify the physiological involvement of endogenous opiates in the steroid-mediated control of gonadotrophin release. Our studies showed that there was an acute reduction in the inhibitory effects of endogenous opiates on LH and FSH release following gonadectomy in the rat. This was indicated by a significant reduction in the ability of naloxone to stimulate serum LH/FSH levels (sampled at 15 min) in 26-day-old female rats 48 h after ovariectomy. Luteinizing hormone was highly sensitive to the inhibitory effects of the synthetic met-enkephalin analogue, FK 33-824, at this time (sampled at 90 min). An unexpected observation was that long-term absence of gonadal steroids also disrupted the ability of exogenous opiates, FK 33-824 and morphine, to influence LH release. This was seen as an inability of FK 33-824 (1·0 or 3·0 mg/kg) to inhibit LH secretion. The effects of gonadectomy on opiate control of LH occurred at all developmental stages and were not due to a disruption of sexual maturation. Opiate involvement in prolactin secretion did not appear to be adversely affected by an absence of gonadal steroids. Another novel aspect of this work was that the opiatergic component in the control of gonadotrophin secretion could be reinstated in long-term gonadectomized rats by treatment with oestradiol benzoate or testosterone propionate. Similarly, priming with increasing dosages of oestradiol benzoate which resulted in progressively lower LH levels gave larger naloxone responses. This steroid–opiate interdependency suggests that the negative feedback influence of gonadal steroids on LH secretion is conveyed, in part, by hypothalamic opiate peptides. Our results therefore provide a neurochemical basis for gonadal steroid negative feedback. J. Endocr. (1984) 102, 133–141

Progesterone does not inhibit the increase in pituitary content of luteinizing hormone after removal of estradiol in the ewe

1988 ◽  
Vol 118 (2) ◽  
pp. 193-198
Author(s):  
C. Tamanini ◽  
M. E. Crowder ◽  
T. M. Nett
Keyword(s):  
Luteinizing Hormone ◽  
Response Curve ◽  
Late Gestation ◽  
Ovarian Steroids ◽  
Term Administration ◽  
Lh Release ◽  
High Concentrations

Abstract. During late gestation in the ewe, the pituitary content of LH is reduced by about 95%, presumably due to the presence of high concentrations of ovarian steroids. The aim of this study was to determine whether the pituitary content of LH in the ewe can increase after long-term administration of ovarian steroids, when only estradiol (E) is removed or if both E and progesterone (P) must be withdrawn to allow synthesis of LH to occur. Ten ovariectomized ewes were treated with implants containing E and P. After 3 weeks of treatment, the E implants were removed from 5 ewes (–E+P) and both steroid implants were removed from the remaining 5 ewes (−E−P). Five ovariectomized ewes received P implants at the beginning of the experiment and these implants were left in place for the duration of the study; 5 ovariectomized ewes served as controls (C). All animals were injected with 100 μg GnRH iv 3, 6 and 9 weeks after the initiation of treatment. The area under the LH-response curve was used as an indication of the pituitary content of LH. All steroid treatments markedly reduced basal levels of LH. LH levels increased only in −E−P ewes, beginning 6 weeks after initiation of the study. After 3 weeks, −E+P and −E−P ewes released less LH (P < 0.05) in response to GnRH than did C ewes, whereas P animals did not differ from controls. LH release in response to GnRH in −E+P and −E−P groups had increased by 6 and 9 weeks and was not different from that of C ewes. After 9 weeks, LH release in P ewes was reduced (P < 0.05) compared with C ewes. These data suggest that, after the pituitary content of LH has been suppressed by ovarian steroids, the presence of P alone does not inhibit replenishment of the pituitary content of LH.

Suppressive effect of prolactin on oestrogen-induced secretion of LH by sequentially perifused rat hypothalamus-pituitary

1985 ◽  
Vol 108 (2) ◽  
pp. 151-155 ◽  
Author(s):  
Jin-Woo Lee ◽  
Akira Miyake ◽  
Keiichi Tasaka ◽  
Shirou Otsuka ◽  
Toshihiro Aono ◽  
...  
Keyword(s):  
Experimental Period ◽  
Suppressive Effect ◽  
Control Group ◽  
Gonadotrophin Secretion ◽  
Lh Release ◽  
Lh Secretion ◽  
Hypothalamic Level ◽  
Experimental Group ◽  
Perifusion System

Abstract. The effect of prolactin (Prl) on oestrogeninduced gonadotrophin secretion was examined in vitro in a sequential double chamber perifusion system. As control groups, mediobasal hypothalamus (MBH)-pituitary pairs or pituitaries without the MBHs were perifused with Medium 199. As an experimental group, MBH-pituitary pairs were perifused with Medium 199 containing 1 μg/ml of rat Prl. These groups were stimulated with 10−7m oestradiol-17β (E2) for 30 min, and luteinizing hormone (LH) in the serial fractions of effluent was measured. In the control group of MBH-pituitary pairs perifused with medium without Prl, secretion of LH began to rise within 30 min after the beginning of stimulation, reached a peak 30 min after the end of stimulation and then remained at a plateau for the rest of the experimental period, whereas in the control group of pituitaries alone no significant response was observed. In the experimental group perifused with medium containing Prl, LH-secretion showed peaks 20 and 80 min after the end of E2-stimulation, respectively, and the first peak was significantly (P < 0.01) less than the level in the control group. These data demonstrate that Prl at this concentration suppressed the rapid LH release induced by E2. Its site of action is suggested to be at the hypothalamic level, and its possible mechanism of action is discussed.

Neuropharmacological analysis of the control of LH secretion in gonadectomized male and female rats: altered hypothalamic responses to inhibitory neurotransmitters in long-term castrated rats

1988 ◽  
Vol 119 (1) ◽  
pp. 15-21 ◽  
Author(s):  
O. F. X. Almeida ◽  
K. E. Nikolarakis ◽  
A. Herz
Keyword(s):  
Opioid Receptor ◽  
Female Rats ◽  
Male Rats ◽  
Dopaminergic Agonists ◽  
Male And Female ◽  
Opioid Agonists ◽  
Male And Female Rats ◽  
Lh Release ◽  
Lh Secretion

ABSTRACT The control of LHRH and LH by neurotransmitters and neuromodulators such as the endogenous opioid peptides is essentially the same in intact adult male and female rats: adrenergic and dopaminergic agonists stimulate LH release and opioid agonists inhibit it. Several weeks after gonadectomy, however, the contribution of the endogenous ligands of adrenergic, dopaminergic and opioidergic receptors to the control of LHRH is altered. A detailed pharmacological analysis in long-term ovariectomized females confirmed previous reports that adrenergic and dopaminergic agonists still enhance secretion of LHRH and LH and opioid receptor agonists still suppress it. A similar investigation in long-term castrated males also confirmed previous reports that opioid agonists fail to block LH secretion. In addition, we have found that while adrenergic and dopaminergic agonists cause increases in serum concentrations of LH, adrenoreceptor and dopamine receptor antagonists do not inhibit LH release in long-term castrates. Furthermore, the opioid antagonist naloxone does not raise serum LH levels in either sex after long-term gonadectomy. These observations therefore imply reduced opioidergic, dopaminergic and adrenergic transmission, in relation to LHRH release, after longterm castration. In addition, opioid receptor activity (assessed by responsiveness to an opioid receptor agonist) of female rats is maintained, whereas that of male rats is lost, after long-term gonadectomy. J. Endocr. (1988) 119, 15–21

Effect of opioid peptides on gonadotrophin secretion

1982 ◽  
Vol 99 (3) ◽  
pp. 321-325 ◽  
Author(s):  
M. Motta ◽  
L. Martini
Keyword(s):  
Opioid Peptides ◽  
Serum Levels ◽  
Ovariectomized Rats ◽  
Intraventricular Injection ◽  
Experimental Conditions ◽  
Serum Lh ◽  
Gonadotrophin Secretion ◽  
Intraventricular Injections ◽  
Lh Release

Abstract. The intraventricular injection of 25 μg of Methionine-Enkephalin (Met-Enk) induces a significant increase of serum LH levels in long-term ovariectomized rats 15, 30 and 60 min following administration. The synthetic Met-Enk agonistic analogue [D-Ala2]Methionine-Enkephalinamide ([D-Ala2]Met-Enk) also enhances significantly serum LH levels at 30 and 60 min; under the same experimental conditions neither Met-Enk nor [D-Ala2]Met-Enk modifies serum levels of FSH following intraventricular injections into ovariectomized animals. It is concluded that, under particular circumstances, opioid peptides of the Met-Enk family may stimulate LH release.

scholarly journals Effects of pregnancy on pulsatile secretion of LH and gonadotrophin-releasing hormone-induced LH release in sheep: a longitudinal study

Reproduction ◽  
2003 ◽  
pp. 347-355 ◽  
Author(s):  
KH Al-Gubory ◽  
J Hervieu ◽  
PA Fowler
Keyword(s):  
Longitudinal Study ◽  
Gnrh Agonist ◽  
Response Curve ◽  
Oestrous Cycle ◽  
Separate Group ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
High Concentrations ◽  
Physiological Dose ◽  
Lh Secretion

Pulsatile LH secretion and its control throughout pregnancy have not been fully determined in sheep. Expt 1 determined the patterns of LH secretion in five ewes on days 10, 20, 60 and 120 of pregnancy and on day 10 postpartum, compared with those on day 10 of the oestrous cycle. Mean (+/- SEM) concentrations of LH declined steadily throughout pregnancy (ANOVA, P < 0.01) and were lower (P < 0.01) on day 60 (0.19 +/- 0.3 ng ml(-1)) and on day 120 (0.18 +/- 0.4 ng ml(-1)) of pregnancy than on day 10 of the oestrous cycle (0.55 +/- 0.04 ng ml(-1)). This decrease was due to a significant reduction in the number and the amplitude of LH pulses. Only on day 120 of pregnancy were progesterone concentrations higher (P < 0.01) than on day 10 of the oestrous cycle. Although concentrations of progesterone on day 10 postpartum were barely detectable, mean LH concentration (0.45 +/- 0.09 ng ml(-1)) was not different from that on day 10 of the oestrous cycle. Expt 2 examined the LH responses in a separate group of four ewes to a physiological dose of GnRH (0.2 microg) on days 10, 20, 60 and 120 of pregnancy and on day 10 postpartum, compared with those on day 10 of the oestrous cycle. The area under the LH response curve and the maximum LH concentrations induced by GnRH declined steadily throughout pregnancy (ANOVA, P < 0.01) and were lower (P < 0.01) on days 60 and 120 of pregnancy than on day 10 of the oestrous cycle, but these parameters were not different between day 10 postpartum and day 10 of the oestrous cycle. Expt 3 examined the LH responses in a separate group of four ewes to a potent GnRH agonist, buserelin (0.5 microg), on days 10, 60 and 120 of pregnancy. The area under the LH response curve and the maximum LH concentrations induced by GnRH were lower (P < 0.01) on days 60 and 120 than on day 10 of pregnancy, but were not different between days 60 and 120. This longitudinal study demonstrates that the pulsatile LH release and pituitary responsiveness to GnRH decreases progressively as pregnancy advances, but does not support the hypothesis that high concentrations of progesterone are solely responsible for the inhibition of pulsatile LH secretion and GnRH-induced LH release during pregnancy in sheep.

Cholinergic inputs to the amygdala and the control of gonadotrophin release

1980 ◽  
Vol 93 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Flavio Piva ◽  
José Borrell ◽  
Patrizia Limonta ◽  
Gilberto Gavazzi ◽  
Luciano Martini
Keyword(s):  
Nicotinic Receptors ◽  
Serum Levels ◽  
Inhibitory Effect ◽  
Female Rats ◽  
Muscarinic Agonist ◽  
Time Intervals ◽  
Gonadotrophin Secretion ◽  
Lh Release ◽  
Lh Secretion ◽  
Cholinomimetic Drugs

Abstract. Adult female rats castrated 4 weeks before were implanted bilaterally into the basomedial area of the amygdala with drugs known to mimic or to counteract the actions of acetylcholine. The animals were sacrificed at different time intervals after the implantation of the different compounds, and serum levels of LH and FSH were measured by radioimmunoasay. The data obtained indicate that the intra-amygdalar implantation of the muscarinic blocker atropine induces a significant increase of the release of LH without altering FSH secretion. The implantation of two cholinomimetic drugs, pilocarpine, an almost pure muscarinic agonist, and carbachol, which possesses both muscarinic and nicotinic properties, exerted an inhibitory effect only on LH release. On the contrary, the intra-amygdalar placement of the nicotinic blocker mecamylamine was followed by an increase of FSH with no changes in LH. These observations may suggest that cholinergic signals reaching the amygdala may be of some relevance in the mechanisms controlling gonadotrophin secretion. Muscarinic receptors seem to play an inhibitory role in the regulation of LH secretion, while nicotinic receptors seem to modulate in an inhibitory way FSH release.

Effects of body condition at calving, post-partum nutrition and calf access on the interval from calving to first ovulation in beef cows: Ovarian folliculogenesis and gonadotrophin secretion

1999 ◽  
Vol 1999 ◽  
pp. 5-5
Author(s):  
M. G. Diskin ◽  
D. R. Mackey ◽  
A. Sanz ◽  
L. Marongiu ◽  
G. Quintans ◽  
...  
Keyword(s):  
Post Partum ◽  
Beef Cows ◽  
Productive Efficiency ◽  
Interactive Effects ◽  
Wave Dynamics ◽  
Follicular Wave ◽  
Gonadotrophin Secretion ◽  
Lh Release ◽  
Ovarian Folliculogenesis ◽  
Lh Secretion

The interval from calving to first ovulation is a major factor affecting reproductive and productive efficiency in beef cows. While this interval is affected by pre- and post-partum nutrition, the maternal-offspring bond is generally considered to be the major cause of delayed ovulation in beef cows. The endocrine and physiological mechanisms by which these factors either singularly or interactively control the duration of the post-partum anovulatory period are not well established, although they most likely involve the regulation of pulsatile LH release. The present study sought to examine the interactive effects of pre- and post-partum nutrition on LH secretion and follicle wave dynamics following acute calf isolation and once-a-day suckling (restricted access), after emergence of the fourth follicular wave post partum.

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