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

Cyclophenil, a non-steroidal compound with a higher central than peripheral oestrogenic activity: study of its effects on uterine growth and on some central parameters in castrated female rats

1984 ◽  
Vol 107 (3) ◽  
pp. 340-345 ◽  
Author(s):  
F. Celotti ◽  
N. Avogadri ◽  
R. C. Melcangi ◽  
S. Milani ◽  
P. Negri-Cesi
Keyword(s):  
Prolactin Secretion ◽  
The Other ◽  
Female Rats ◽  
Reliable Estimate ◽  
Growth Test ◽  
Oestradiol Benzoate ◽  
Enzymatic Systems ◽  
Uterine Growth ◽  
Steroidal Compound

Abstract. The oestrogenic activity of cyclophenil, a non-steroidal compound which has structural analogies with both stilbene and triphenylethylene, has been reevaluated utilizing both central and peripheral parameters. The central parameters considered were LH, FSH, prolactin secretion and two enzymatic systems known to be oestrogen-sensitive: hypophyseal 5α-reductase and hypothalamic aromatase. The uterine growth test was used to determine oestrogenic peripheral activity. The compound was administered at various doses in comparison with oestradiol benzoate (EB) to long-term castrated female rats. Cyclophenil has an activity 1/8110 times that of EB on uterine growth, and 1/1660 and 1/550 times that of EB in inhibiting LH and FSH. respectively. The hypophyseal 5α-reductase(expressed as DHT formation) was inhibited 1710 times less by cyclophenil than by EB. The other parameters considered were unsuitable to provide a statistically reliable estimate of the potency ratios between the two compounds. The data show that cyclophenil is an oestrogenic compound with peculiar characteristics. This substance is more effective in expressing its oestrogenic activity in central structures than in the peripheral ones.

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

Retardation of preovulatory desensitization to negative oestrogen feedback: mechanism of the effect of progesterone in 5-day cyclic rats

1987 ◽  
Vol 114 (3) ◽  
pp. 409-414 ◽  
Author(s):  
F. Döcke ◽  
W. Rohde ◽  
R. Chaoui ◽  
J. Stürzebecher ◽  
G. Dörner
Keyword(s):  
Preoptic Area ◽  
Feedback Mechanism ◽  
Ovarian Cycle ◽  
Female Rats ◽  
Mediobasal Hypothalamus ◽  
Inhibiting Effect ◽  
Gonadotrophin Secretion ◽  
Oestradiol Benzoate ◽  
Lh Secretion ◽  
Follicle Maturation

ABSTRACT Recent studies have shown that oestrogen can induce desensitization to its own gonadotrophin-inhibiting effect in female rats by an action on the medial preoptic area (MPOA). Probably as a consequence of this action, sensitivity to the negative oestrogen feedback declines markedly between metoestrus and dioestrus of the 4-day ovarian cycle. To study this desensitization process in 5-day cyclic rats, females exhibiting regular 5-day vaginal cyclicity were ovariectomized on consecutive days of the cycle, injected with oestradiol benzoate (OB) or oil on the day of ovariectomy and autopsied 24 h after the injection. Estimation of the serum concentration of LH revealed that desensitization to negative oestrogen feedback occurred only between day 2 of dioestrus and pro-oestrus, i.e. 2 days later than in females with a 4-day cycle. In the latter animals, an injection of progesterone in metoestrus or early dioestrus, which induced lengthening of the ovarian cycle for 1 day, delayed the onset of desensitization to a degree similar to that found in spontaneously 5-day cyclic rats. In acutely ovariectomized females, progesterone implants placed in the MPOA, but not those located in the mediobasal hypothalamus, increased the LH-inhibiting effect of low doses of OB. The results suggest that the prolonged secretion of progesterone recorded in 5-day cyclic rats retards follicle maturation and delays the forthcoming ovulation by acting, at least partly, on the MPOA and antagonizing the desensitizing effect of oestrogen. In this way, inhibition of gonadotrophin secretion by oestrogen is enhanced and the increase in tonic LH secretion necessary for the completion of follicle maturation is retarded. J. Endocr. (1987) 114, 409–414

Effects of gonadal steroids on the opioid regulation of LH and prolactin release in ovariectomized pony mares

1995 ◽  
Vol 147 (2) ◽  
pp. 195-202 ◽  
Author(s):  
C Aurich ◽  
P F Daels ◽  
B A Ball ◽  
J E Aurich
Keyword(s):  
Prolactin Secretion ◽  
Gonadal Steroids ◽  
Opioid Antagonist ◽  
Regulatory Pathway ◽  
Prolactin Release ◽  
Oestradiol Benzoate ◽  
Significant Release ◽  
Lh Secretion ◽  
Opioid Systems

Abstract The aim of the present study was to investigate the role of ovarian steroids in the opioid regulation of LH and prolactin release in mares. Effects of the opioid antagonist naloxone on LH and prolactin secretion were determined in ovariectomized pony mares. The animals were pretreated with either progesterone (500 μg kg−1) or oestradiol benzoate (10 μg kg−1) for 8 days and subsequently with a combination of progesterone and oestradiol for an additional 8 days. Naloxone administration (0·5 mg kg−1 i.v.) resulted in a significant release of LH as well as prolactin in mares after pretreatment with either oestradiol benzoate or progesterone plus oestradiol benzoate (P<0·05). No significant changes in LH and prolactin secretion were detected in progesterone-treated and non-steroid-treated ovariectomized mares. These results indicate that a prolonged oestrogen influence activates the opioid inhibition of LH and prolactin release in mares. In contrast to other species, progesterone alone does not activate a tonic opioid inhibition of LH and prolactin secretion, but modulates the effect of oestrogens. The opioid systems therefore seem to be regulated by a sequence of different steroid environments, as found during the oestrous cycle. The parallel increases in prolactin and LH secretion in mares may indicate a common regulatory pathway for these two hormones. Journal of Endocrinology (1995) 147, 195–202

EFFECT OF GONADECTOMY AND OESTROGEN ON PITUITARY LH-CONTENT AND ORGAN WEIGHTS IN ANDROGEN-STERILIZED FEMALE RATS

1966 ◽  
Vol 52 (3) ◽  
pp. 471-477 ◽  
Author(s):  
G. P. van Rees ◽  
E. Gans
Keyword(s):  
Negative Feedback ◽  
Chronic Treatment ◽  
Testosterone Propionate ◽  
Female Rats ◽  
Feedback Mechanisms ◽  
Ovarian Steroids ◽  
Organ Weights ◽  
Normal Manner ◽  
Oestradiol Benzoate ◽  
Lh Secretion

ABSTRACT In female rats sterilized by an injection of testosterone propionate (TP) shortly after birth, the effects of gonadectomy and gonadectomy plus chronic treatment with oestradiol benzoate were studied. Pituitary LH-contents were affected in a similar way as in normal females, although there was an indication that the sensitivity of the response of pituitary LH-content to oestradiol was slightly less in TP-sterilized than in normal rats. The effect of oestradiol on uterine weights was definitely less in gonadectomized TP-sterilized rats than in gonadectomized controls. It was therefore concluded that negative feedback mechanisms between ovarian steroids and LH-secretion operate in a normal manner in TP-sterilized rats. The sensitivity of the uterus to oestrogen, however, is decreased.

OESTROGEN AND PROGESTERONE INFLUENCE ON THE RELEASE OF PROLACTIN IN OVARIECTOMIZED RATS

1974 ◽  
Vol 60 (2) ◽  
pp. 205-215 ◽  
Author(s):  
L. CALIGARIS ◽  
J. J. ASTRADA ◽  
S. TALEISNIK
Keyword(s):  
Single Injection ◽  
Prolactin Secretion ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Inhibitory Effects ◽  
Oestradiol Benzoate ◽  
Close Relationship ◽  
Dose Dependent

SUMMARY The concentration of prolactin in serum after oestrogen and progesterone injection into spayed rats was measured by radioimmunoassay. After a single injection of 5 μg oestradiol benzoate (OB) into long-term ovariectomized rats, serum prolactin concentrations showed a circadian rhythm with high levels in the afternoon and almost no changes in the morning. Peaks of prolactin occurred 2, 3 and 4 days after the injection. Below a dose of 1 μg OB, the response was dose-dependent, but the response was then maximal. In spayed rats primed with 5 μg OB, the injection of 2 mg progesterone 2, 3 or 4 days later resulted in a significant increase in serum prolactin. This response, in contrast to that of oestrogen, occurred in the morning and in the evening and was found to be dose-dependent. The rise in serum prolactin after injection of 1 mg progesterone also showed a close relationship to the priming dose of OB. Progesterone had no effect in spayed, untreated animals. Maximal levels of prolactin were attained 3–4 h after the s.c. injection of progesterone. The release of prolactin which can be induced either by OB or by progesterone was blocked by the administration of progesterone injected 1 day before the expected release would occur. These results indicate that progesterone exerts both facilitatory and inhibitory effects on prolactin secretion. Male rats were found to be less sensitive to the ovarian steroid treatment. It is suggested that oestrogen could be responsible for the rise in prolactin observed at pro-oestrus and progesterone for the increase in prolactin in pseudopregnancy and pregnancy.

The depressing (negative) effect of oestradiol benzoate on the in vitro secretion of LH and FSH by the pituitary gland of the LRH-pretreated long-term ovariectomized rat changes into the augmentative (positive) effect after discontinuation of the LRH-pretreatment

1985 ◽  
Vol 110 (3) ◽  
pp. 329-337 ◽  
Author(s):  
G. A. Schuiling ◽  
H. Moes ◽  
T. R. Koiter
Keyword(s):  
Depressing Effect ◽  
Ovx Rats ◽  
Gonadotrophin Secretion ◽  
Oestradiol Benzoate ◽  
Negative Effect ◽  
Positive Effect ◽  
Perifusion System

Abstract. The effect of pretreatment in vivo with oestradiol benzoate on in vitro secretion of LH and FSH was studied in long-term ovariectomized (OVX) rats both at the end of a 5-day continuous in vivo pretreatment with LRH and 4-days after cessation of such LRH pretreatment. Rats were on day 0 sc implanted with osmotic minipumps which released LRH at the rate of 250 ng/h. Control rats were implanted with a piece of silicone elastomer with the dimensions of a minipump. On days 2 and 4 the rats were injected with either 3 μg EB or with oil. On day 5 part of the rats were decapitated and the in vitro autonomous (i.e. non-LRH-stimulated) and 'supra-maximally' LRHstimulated release of LH and FSH was studied using a perifusion system. From other rats the minipumps were removed on day 5 and perifusion was performed on day 9. On the 5th day of the in vivo LRH pretreatment the pituitary LH/FSH stores were partially depleted; the pituitaries of the EB-treated rats more so than those of the oil-injected rats. EB alone had no significant effect on the content of the pituitary LH- and FSH stores. On day 9, i.e. 4 days after removal of the minipumps, the pituitary LH and FSH contents had increased in both the oil- and the EB injected rats, but had not yet recovered to control values. In rats not subjected to the 5-days pretreatment with LRH EB had a positive effect on the supra-maximally LRH-stimulated secretion of LH and FSH as well as on the non-stimulated secretion of LH. EB had no effect on the non-stimulated secretion of FSH. After 5 days of in vivo pretreatment with LRH only, the in vitro non-stimulated and supra-maximally LRH-stimulated secretion of both LH and FSH were strongly impaired, the effect correlating well with the LRH-induced depletion of the pituitary LH/FSH stores. In such LRH-pretreated rats EB had on day 5 a negative effect on the (already depressed) LRH-stimulated secretion of LH (not on that of FSH). EB had no effect on the non-stimulated LH/FSH secretion. It could be demonstrated that the negative effect of the combined LRH/EB pretreatment was mainly due to the depressing effect of this treatment on the pituitary LH and FSH stores: the effect of oestradiol on the pituitary LRH-responsiveness (release as related to pituitary gonadotrophin content) remained positive. In LRH-pretreated rats, however, this positive effect of EB was smaller than in rats not pretreated with LRH. Four days after removal of the minipumps there was again a positive effect of EB on the LRH-stimulated secretion of LH and FSH as well as on the non-stimulated secretion of LH. The positive effect of EB on the pituitary LRH-responsiveness was as strong as in rats which had not been exposed to exogenous LRH. The non-stimulated secretion of FSH was again not affected by EB. The results demonstrate that the effect of EB on the oestrogen-sensitive components of gonadotrophin secretion consists of two components: an effect on the pituitary LRH-responsiveness proper, and an effect on the pituitary LH/FSH stores. The magnitude of the effect of EB on the LRH-responsiveness is LRH dependent: it is very weak (almost zero) in LRH-pretreated rats, but strong in rats not exposed to LRH as well as in rats of which the LRH-pretreatment was stopped 4 days previously. Similarly, the effect of EB on the pituitary LH and FSH stores is LRH-dependent: in the absence of LRH, EB has no influence on the contents of these stores, but EB can potentiate the depleting effect of LRH on the LH/FSH-stores. Also this effect disappear after cessation of the LRH-pretreatment.

GONADAL HORMONES AND THE CONTROL OF OVULATION IN THE GUINEA-PIG

1972 ◽  
Vol 55 (3) ◽  
pp. 599-607 ◽  
Author(s):  
B. T. DONOVAN ◽  
A. N. LOCKHART
Keyword(s):  
Guinea Pig ◽  
Corpus Luteum ◽  
Acute Treatment ◽  
Gonadal Hormones ◽  
Time Of Day ◽  
Gonadal Steroids ◽  
Corpora Lutea ◽  
Plasma Progesterone ◽  
Gonadotrophin Secretion ◽  
Oestradiol Benzoate

SUMMARY The release of ovulating hormone after acute treatment with gonadal steroids, or corpus luteum removal on different days of the oestrous cycle, was studied in the guinea-pig. Injection of 25, 50 or 100 μg oestradiol or 2·5 mg progesterone on day 13 of the cycle had no effect upon gonadotrophin secretion as judged by follicular histology, but markedly altered the sizes of the corpora lutea of the previous ovulation. Treatment with oestradiol on day 14 did not elicit gonadotrophin secretion. However, administration of the same hormones to animals given 10 μg oestradiol benzoate 24 h earlier caused ovulation or follicular luteinization. Progesterone (2·5 mg) appeared least effective in stimulating gonadotrophin release; 25 μg oestradiol were more effective when given at 12.00 h than at 24.00 h but treatment with both hormones caused ovulation when given at either time of day. Luteal volumes were not affected. Removal of corpora lutea during the second half of the cycle advanced the time of expected ovulation to day 15 or earlier when the procedure was carried out on days 8 or 9, but not on days 10–13. It is concluded that 4–5 days must elapse between the fall in plasma progesterone level associated with corpus luteum regression and the release of ovulating hormone.

PHOTOPERIODIC MODULATION OF GONADOTROPHIN SECRETION IN CASTRATED JAPANESE QUAIL

1982 ◽  
Vol 92 (1) ◽  
pp. 73-83 ◽  
Author(s):  
H. F. URBANSKI ◽  
B. K. FOLLETT
Keyword(s):  
Japanese Quail ◽  
Plasma Levels ◽  
Time Course ◽  
Neural Mechanisms ◽  
Gonadal Steroids ◽  
Photoperiodic Control ◽  
Gonadotrophin Secretion ◽  
Lh Secretion ◽  
Sexually Mature ◽  
Short Days

Male Japanese quail were castrated when sexually immature and immediately exposed to one of the following stimulatory lighting regimes for 52 days: 11 h light: 13 h darkness/day (11L : 13D), 12L : 12D, 13L : 11D, 14L : 10D, 15L : 9D, 16L : 8D, 20L : 4D or 23L : 1D. One group was retained on short days (8L : 16D). Clearcut differences in the plasma levels of LH and FSH emerged between the various groups. Levels remained very low in castrated quail on 8L : 16D but were much greater in those on 14L : 10D, 15L : 9D, 16L : 8D, 20L : 4D and 23L : 1D, eventually becoming 15 to 20 times higher. Less pronounced castration responses developed on 13L : 11D, 12L : 12D or 11L : 13D. Alterations in photoperiod after day 52 caused an appropriate rise or fall in LH secretion. Photoperiodically induced suppressions were rapid, being highly significant within 4 days, but increases usually had a slower time course. When sexually mature quail (on 16L : 8D) were castrated and transferred to 8L : 16D they also exhibited a rapid suppression in LH secretion. Thus in quail, unlike some mammals, the photoperiodic control over gonadotrophin secretion is independent of the reproductive status of the animal at the time of castration. The results confirm the view that changes in sensitivity of the hypothalamo-pituitary axis to gonadal steroids are not a primary factor in the neural mechanisms underlying photoperiodism in quail.

SENSITIVITY OF ANTERIOR HYPOTHALAMIC AREAS TO GONADAL STEROID IMPLANTATION IN ANDROGENIZED FEMALE RATS

1977 ◽  
Vol 74 (2) ◽  
pp. 315-NP ◽  
Author(s):  
A. DANGUY ◽  
J. L. PASTEELS ◽  
F. ECTORS
Keyword(s):  
Single Injection ◽  
Mammary Glands ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Male Rats ◽  
Control Synthesis ◽  
Normal Female ◽  
Immunofluorescence Studies ◽  
Oestradiol Benzoate ◽  
Stimulation Of

A single injection of 1 mg of a complex of testosterone esters on day 5 of life was used to prepare constantly oestrous rats. Such androgenized female rats were then ovariectomized and submitted to stereotaxical implantation of 1 μg oestradiol benzoate, 5 μg testosterone isobutyrate or, as a control, 10 μg cholesterol in the anterior hypothalamic areas. The effects of the steroids on plasma and pituitary FSH and LH were assessed by radioimmunoassay. As reported previously by us in normal female and male rats, the preoptic–suprachiasmatic area (POA) was able to control synthesis and secretion of both gonadotrophins and did not lose its sensitivity to oestradiol and testosterone in androgenized rats. Evidence for enhanced prolactin secretion in androgenized rats was derived from immunofluorescence studies of the pituitary gland and from histology of the mammary glands. In this respect the condition of the androgenized females was opposite to that of the males. The present work demonstrated that stimulation of prolactin secretion in androgenized female rats resulted from oestrogen action due to permanent oestrus rather than from impairment of hypothalamo-hypophysial relationships. Indeed, prolactin stimulation was suppressed when the androgenized rats were ovariectomized and restored when they were subsequently implanted with oestradiol in the POA.

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