Morphine can stimulate prolactin release independent of a dopaminergic mechanism

1988 ◽  
Vol 66 (11) ◽  
pp. 1381-1385 ◽  
Author(s):  
S. H. Shin ◽  
M. C. Obonsawin ◽  
D. A. Van Vugt ◽  
N. Baby ◽  
K. Jhamandas
Keyword(s):  
Large Dose ◽  
Rat Plasma ◽  
Morphine Sulfate ◽  
Male Rats ◽  
Normal Male ◽  
Plasma Prolactin ◽  
Dopaminergic Receptors ◽  
Prolactin Release ◽  
Inhibiting Factor ◽  
Dopaminergic Mechanism

Prolactin release is controlled by prolactin-release inhibiting factor (PIF), possibly dopamine, and an unidentified putative hypothalamic prolactin-releasing factor (PRF). Morphine and related opioids may indirectly stimulate prolactin release by inhibiting PIF release and (or) by stimulating putative PRF release. In the present study, we have completely blocked the dopaminergic receptors in normal male rats by pretreatment with a large dose of pimozide (3 mg/kg) to demonstrate if putative PRF has a role in morphine-induced prolactin release. Morphine sulfate (10 mg/kg) was still able to stimulate prolactin release in the rat without any functional dopaminergic PIF receptors. When naloxone (3 mg/kg) was injected 20 min before the morphine in the pimozide-treated rat, plasma prolactin concentration was not affected by morphine indicating that the stimulatory effect of this opioid on prolactin release in the pimozide-pretreated rat was mediated by μ-receptors. We can conclude that morphine can stimulate prolactin release through a mechanism apparently independent of dopaminergic receptors, one possible route being through a putative PRF.

PROLACTIN STIMULATION TEST WITH PERPHENAZINE: AN EVALUATION OF PLASMA PROLACTIN LEVELS AND PITUITARY SECRETORY ACTIVITY IN THE RAT

1976 ◽  
Vol 68 (3) ◽  
pp. 355-368 ◽  
Author(s):  
A. A. VAN DER GUGTEN ◽  
P. C. SAHULEKA ◽  
G. H. VAN GALEN ◽  
H. G. KWA
Keyword(s):  
Adult Male ◽  
Secretory Activity ◽  
Female Rats ◽  
Male Rats ◽  
Plasma Prolactin ◽  
Prolactin Release ◽  
Oestrogen Treatment ◽  
Endocrine Status ◽  
Pituitary Prolactin ◽  
Single Plasma

SUMMARY Many investigations of the regulation of prolactin synthesis and release are based on single plasma prolactin determinations. The purpose of the present experiment was to ascertain whether groups of rats (i.e. young or adult, male or female animals, being either intact, gonadectomized or gonadectomized and treated with oestrone), differing in age and/or endocrine status, will react to a single dose of perphenazine by an acute release of pituitary prolactin in proportion to their initial plasma prolactin levels. No consistent relation existed between the classification of the twelve groups of rats into three categories of basal plasma prolactin levels (i.e. < 20, 25–50, > 125 ng/ml) and their response to perphenazine. Even though all groups showed a highly significant increase of plasma prolactin levels the magnitude of the maximum prolactin response at 30 min varied greatly within the groups of one category and thus was not related to the initial prolactin levels. The effect of 14 days of oestrone treatment in increasing plasma prolactin levels in gonadectomized animals was greatest in young and adult male rats, less in young females and not significant in adult females. The results obtained after perphenazine treatment in the latter group made it clear that the effect of oestrogen treatment on prolactin release can be completely blocked by increasing synthesis and/or release of the prolactin-release inhibiting factor (PIF). Since perphenazine induces decrease of pituitary prolactin and a concomitant increase of plasma prolactin levels through lowered PIF-action, the positive effect of oestrogens on prolactin release (as observed in gonadectomized male and young female rats) apparently is caused by a different mode of action. The implications of these findings for the regulation of prolactin release, as affected by the endocrine status of the rat, is discussed. Moreover, comparison of prolactin lost from the pituitary and gained in the circulation of the experimental animals, with amounts of prolactin that were observed to disappear from plasma during the experiment, provided suggestive evidence that the capacity to synthesize and/or eliminate prolactin, after a sudden provoked release of the hormone, differed among the groups. The rates of synthesis by the pituitary, of release from the pituitary into the circulation as well as of elimination of the hormone from the circulation (equally involved in determining actual plasma levels) are thought, therefore, to be far more important for the elucidation of prolactin regulation than single plasma prolactin determinations.

Postreceptorial refractoriness of prolactin release mechanisms

1983 ◽  
Vol 61 (7) ◽  
pp. 676-684 ◽  
Author(s):  
R. Collu ◽  
J. R. Ducharme ◽  
D. Eljarmak ◽  
A. M. Marchisio ◽  
J. Bertrand ◽  
...  
Keyword(s):  
Binding Sites ◽  
Immobilization Stress ◽  
Significant Rise ◽  
Male Rats ◽  
Plasma Prolactin ◽  
Initial Value ◽  
Prolactin Release ◽  
Pituitary Glands ◽  
Plasma Prl

Whilc a first injection of the antidopaminergic benzamide drug, sulpiride, induced a large rise in plasma prolactin (PRL) levels in chronically cannulated adult male rats, a second injection given 2 h later was totally inactive although the pituitary content of the hormone was still 76% of the initial value. When the second injection was given 8 h after the first it was slightly effective, but when administered 24 h later it was as effective as the first. The second of two consecutive injections of haloperidol given at 2-h intervals, or an injection of morphine given 2 h after sulpiride, were incapable of inducing a release of PRL. Two hours after an injection of sulpiride, a 30-min period of immobilization stress induced a significant rise in plasma PRL levels. A significant rise in plasma PRL levels was also observed when larger doses of sulpiride were given 2 h after a first injection of the drug. Apomorphine was at least as effective an inhibitor of PRL secretion when given 2 h after sulpiride than when injected after saline. In vitro studies of dopaminergic binding sites revealed the presence, in pituitary glands of sulpiride-treated rats, of receptors not modified by the drug. These data suggest that the only plausible explanation for the ineffectiveness of the second of two consecutive injections of sulpiride is the development of a state of refractoriness of the mechanisms that subserve the release of PRL induced by suppression of the inhibitory dopaminergic tonus.

Bovine neurophysin-II stimulates prolactin release without involvement of dopaminergic prolactin-release inhibiting factor receptor in the estradiol-primed male rat

1989 ◽  
Vol 121 (3) ◽  
pp. 411-416
Author(s):  
S. H. Shin ◽  
M. C. Obonsawin ◽  
R. Stirling
Keyword(s):  
Blocking Agent ◽  
Male Rats ◽  
Male Rat ◽  
Prolactin Release ◽  
Inhibiting Factor ◽  
Inert Carrier ◽  
A Chain ◽  
Neurophysin Ii ◽  
Factor Release ◽  
Stimulation Of

Abstract. Neurophysins have been considered to be physiologically inert carrier proteins for the neurohypophysial hormones, oxytocin and vasopressin. We have observed that bovine neurophysin-II indirectly stimulates prolactin release in estradiol-primed male rats. The release of prolactin is regulated by a dual hypothalamic control system, the prolactin-release-inhibiting factor and the prolactin-releasing factor. We have tried to clarify whether neurophysin-II is acting through stimulation of prolactin-releasing factor by eliminating the possibility of dopaminergic prolactin release-inhibiting factor release. Male rats were primed with estradiol and functional dopaminergic prolactin release-inhibiting factor receptors were completely blocked by pretreatment with a large dose of pimozide (3 mg/kg), a dopaminergic receptor blocking agent. The neurophysin-II stimulated prolactin release in the rats which did not have any functional dopaminergic prolactin release-inhibiting factor receptors suggesting that neurophysin-II likely initiates a chain of events which eventually stimulates prolactin-releasing factor release since the possibility of involvement of the dopaminergic prolactin release-inhibiting factor system is eliminated. Opioids are known to be one of a chain of events which transmit external stress into a stimulation of prolactin release. Naloxone, a μ-receptor antagonist, was injected 20 min before neurophysin-II administration into rats which were primed with estradiol and pretreated with pimozide (3 mg/kg), but the naloxone administration did not block the prolactin release stimulated by neurophysin-II injection. This result indicates that opioids are not one of the chain of events between initiation of stimulation by neurophysin-II and prolactin release.

Decrease of morphine-induced prolactin release by a procedure causing prolonged stress

1984 ◽  
Vol 101 (2) ◽  
pp. 169-172 ◽  
Author(s):  
M. I. K. Fekete ◽  
B. Kanyicska ◽  
T. Szentendrei ◽  
Á. Simonyi ◽  
E. Stark
Keyword(s):  
Large Dose ◽  
Prolactin Secretion ◽  
Prolonged Release ◽  
Plasma Prolactin ◽  
Endogenous Opioid ◽  
Prolactin Release ◽  
Prolonged Immobilization ◽  
Prolonged Stress

ABSTRACT The effects of morphine and fentanyl on plasma prolactin levels in rats have been measured. It was found that a prolonged immobilization stressful procedure for 5 h inhibited the response to morphine and fentanyl to increase prolactin secretion, but did not influence the increase in plasma prolactin caused by haloperidol. The injection of a large dose of cortisol (25 mg/kg, s.c.) also evoked an inhibition of morphine-induced prolactin release. The inhibition was maximal 24 h after the administration of the glucocorticoid. These results indicate that stress may induce prolonged alteration in endogenous opioid-mediated neuro-modulation via a prolonged release of glucocorticoids. J. Endocr. (1984) 101, 169–172

Serotonin stimulates prolactin secretion in the hypophysectomized adenohypophyseal grafted rat

1983 ◽  
Vol 102 (4) ◽  
pp. 511-516 ◽  
Author(s):  
K. M. Stobie ◽  
S. H. Shin
Keyword(s):  
Prolactin Secretion ◽  
Male Rats ◽  
Normal Male ◽  
Plasma Prolactin ◽  
Site Of Action ◽  
Plasma Prl ◽  
Dose Dependent Increase ◽  
Dose Dependent

Abstract. Normal male, oestrogen (E2) primed male and hypophysectomized adenohypophyseal grafted male rats (HAG rats) were used in the experiments. Serotonin creatinine sulphate was injected as a bolus via an indwelling atrial cannula in the conscious free moving rat. Serotonin caused a dose-dependent increase in plasma prolactin (Prl) in normal (1, 3 and 10 mg/kg serotonin) and E2 primed (1 and 3 mg/kg serotonin) male rats that began immediately after injection and reached a peak within 12–15 min of injection. Oestrogen priming significantly increased the magnitude of the response to serotonin. To analyze the site of action of serotonin in the rat, serotonin (1 mg/kg) was injected into HAG rats. Serotonin increased plasma Prl in this rat preparation, indicating that serotonin acts directly on the ectopic pituitary.

Effects of naloxone and neonatal treatment with monosodium-l-glutamate on growth hormone and prolactin release induced by electrical stimulation of the medial-basal hypothalamus in rats

1983 ◽  
Vol 96 (3) ◽  
pp. 427-432 ◽  
Author(s):  
F. A. Antoni ◽  
B. Kanyicska ◽  
G. B. Makara
Keyword(s):  
Electrical Stimulation ◽  
Arcuate Nucleus ◽  
Endogenous Opioids ◽  
Secretory Response ◽  
Male Rats ◽  
Plasma Prolactin ◽  
Prolactin Release ◽  
Medial Basal Hypothalamus ◽  
Neonatal Treatment ◽  
Stimulation Of

The role of nerve cells of the arcuate nucleus and endogenous opioid peptides in the regulation of GH and prolactin secretion has been investigated. Electrical stimulation of the medial-basal hypothalamus (MBH) for 10 min raised plasma levels of both hormones in male rats anaesthetized with pentobarbitone sodium. Plasma hormone levels increased within 5 min after the termination of the stimulus, while no marked changes were found during stimulation. The GH response to the electrical stimulus was substantially reduced in rats with arcuate lesions induced by neonatal treatment with monosodium-l-glutamate (MSG). By contrast, the size of the prolactin response was not altered by MSG treatment. The opiate receptor antagonist naloxone (10 mg/kg, i.v.) failed to influence GH secretion induced by electrical stimulation in either control or MSG-treated animals. The post-stimulus rise of plasma prolactin levels was attenuated by naloxone in control rats, while the same dose of the drug was ineffective in rats which had been exposed to MSG. We conclude that endogenous opioids participate in the increase of prolactin release upon electrical stimulation of the MBH but are not involved in the GH secretory response. Arcuate neurones are important in the maintenance of the GH response to electrical stimulation. By contrast, lesioning of the arcuate nucleus failed to affect the prolactin secretory response elicited by MBH stimulation. However, prolactin release in MSG-treated rats appeared less susceptible to the inhibitory action of naloxone, suggesting a possible supersensitivity towards endogenous opioids.

INFLUENCE OF RESERPINE ON THE PITUITARY CONTENT OF MELANOCYTE-STIMULATING HORMONE AND ON HYPOTHALAMIC FACTORS WHICH AFFECT ITS RELEASE

1968 ◽  
Vol 42 (4) ◽  
pp. 505-512 ◽  
Author(s):  
MARIA E. TOMATIS ◽  
S. TALEISNIK
Keyword(s):  
Median Eminence ◽  
Normal Values ◽  
Male Rats ◽  
Normal Male ◽  
Melanocyte Stimulating Hormone ◽  
Inhibiting Factor ◽  
Pituitary Glands ◽  
Stimulating Hormone

SUMMARY The melanocyte-stimulating hormone (MSH) content of whole toad pituitary glands decreased upon treatment with reserpine. With daily injections the values remained low for 1 week but regained normal levels after 2 weeks in spite of an increased secretion of MSH as indicated by darkening of the skin. In rats a drop in pituitary MSH content also occurred after reserpine injection but normal values were found after 7 and 14 days of treatment. MSH-releasing factor found in stalk-median eminence tissue of normal male rats was not present in the reserpine-injected animals, but after 7 days of treatment an increase in MSH-release-inhibiting factor (MSH-R-IF) was demonstrated. MSH-R-IF was also found to have increased in female castrated rats after 2 days of treatment with reserpine. It is concluded that reserpine permits the secretion of pituitary MSH by blocking the release of MSH-R-IF, which accumulates in the hypothalamic neurones.

PLASMA PROLACTIN IN UNDISTURBED CANNULATED MALE RATS; EFFECTS OF PERPHENAZINE, FREQUENT SAMPLING, STRESS AND CASTRATION PLUS OESTRONE TREATMENT

1977 ◽  
Vol 84 (1) ◽  
pp. 51-61 ◽  
Author(s):  
John A. M. Mattheij ◽  
Thea A. van Pijkeren
Keyword(s):  
Significant Rise ◽  
Male Rats ◽  
Similar Response ◽  
Plasma Prolactin ◽  
Prolactin Release ◽  
Free Sample ◽  
Normal Males ◽  
Plasma Prl ◽  
Frequent Sampling ◽  
Chronic Cannulation

ABSTRACT Blood was collected from undisturbed male rats by means of chronically indwelling intrajugular cannulae and the plasma prolactin (PRL) concentration was determined by a radioimmunoassay. The effect of perphenazine, frequent bleeding, handling and brief ether stress in normal males and of stress in castrated oestrone treated males was determined. The plasma PRL concentration in undisturbed intact males was low. Castration plus oestrone treatment for 3 or 7 weeks had little or no effect on the PRL concentration. Neither frequent blood sampling nor removal of 3 ml blood over a period of 5 h affected plasma PRL concentration. Intravenous administration of perphenazine caused a striking and prolonged increase in plasma PRL in intact males. Brief handling or mild ether stress caused a significant rise in PRL within 2 min in intact males; 15–20 min later PRL had returned to the undisturbed level. Brief ether stress in oestrone treated castrates induced a comparable pattern of prolactin release, although of greater magnitude. In these animals a second stress one hour later induced a similar response. It is concluded that chronic cannulation neither affects the unstressed prolactin level nor interferes with the ability of the adenohypophysis to release PRL. The results also indicate that when rats are handled a truly stress free sample can only be obtained when the blood is drawn within one minute after the initial disturbance of the animal. The evidence presented indicates that oestrone treatment increases the responsiveness of male rats to stress-induced PRL release.

DER EINFLUSS VON RESERPIN AUF DIE ANTITHYREOIDALE WIRKUNG VON KALIUMPERCHLORAT

1962 ◽  
Vol 39 (3) ◽  
pp. 423-430
Author(s):  
H. L. Krüskemper ◽  
F. J. Kessler ◽  
E. Steinkrüger
Keyword(s):  
Thyroid Gland ◽  
Male Rats ◽  
Normal Male ◽  
Tissue Respiration ◽  
List Type ◽  
Morphological Alterations ◽  
Hormone Synthesis ◽  
Stimulation Of

ABSTRACT 1. Reserpine does not inhibit the tissue respiration of liver in normal male rats (in vitro). 2. The decrease of tissue respiration of the liver with simultaneous morphological stimulation of the thyroid gland after long administration of reserpine is due to a minute inhibition of the hormone synthesis in the thyroid gland. 3. The morphological alterations of the thyroid in experimental hypothyroidism due to perchlorate can not be prevented with reserpine.

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