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.

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.

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.

FAILURE OF SODIUM LOADING OR DEFICIENCY TO AFFECT PLASMA PROLACTIN IN THE MALE RAT

1977 ◽  
Vol 86 (2) ◽  
pp. 299-305 ◽  
Author(s):  
J. A. M. Mattheij
Keyword(s):  
Adult Male ◽  
Plasma Aldosterone ◽  
Male Rats ◽  
Male Rat ◽  
Sodium Balance ◽  
Plasma Prolactin ◽  
Deficient Diet ◽  
Marked Rise ◽  
Sodium Metabolism ◽  
Plasma Prl

ABSTRACT The relation between plasma prolactin (PRL) and sodium metabolism was studied in adult male rats. During the experiments attention was given to the avoidance of stress. Cannulated rats were infused with 2.5 ml 5 % NaCl over a 40 min period. Plasma PRL did not change during or up to 2 h after this infusion. Other rats were subjected to a sodium deficient diet for 3 weeks. This treatment which induced a marked rise in plasma aldosterone, did not cause a change in plasma PRL. It is concluded that PRL does not have an important role in the regulation of sodium balance.

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.

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.

Effect of [Asu,]eel calcitonin on prolactin release in normal subjects and patients with prolactinoma

1985 ◽  
Vol 108 (3) ◽  
pp. 297-304 ◽  
Author(s):  
Hidesuke Kaji ◽  
Kazuo Chihara ◽  
Naoto Minamitani ◽  
Hitoshi Kodama ◽  
Tetsuya Kita ◽  
...  
Keyword(s):  
Body Weight ◽  
Bolus Injection ◽  
Normal Subjects ◽  
Regular Insulin ◽  
Prolactin Release ◽  
Saline Administration ◽  
The Central Nervous System ◽  
Plasma Prl ◽  
Male Subjects

Abstract. The effect of [Asu]eel calcitonin (ECT), an equipotent analogue of eel CT, on prolactin (Prl) secretion was examined in 12 healthy male subjects and in 6 patients with prolactinoma. In healthy subjects, ECT (0.5 μg/kg body weight · h) or saline was infused for 2 h and TRH was injected iv as a bolus of 500 μg at 1 h of ECT or saline administration. ECT did not affect basal Prl levels during 1 h of infusion. TRH caused a significant increase of plasma Prl with peak values of 75.2 ± 11.6 ng/ml in ECT-infused subjects, which did not differ from those infused with saline (68.5 ± 8.3 ng/ml). Next, an iv bolus injection of regular insulin (0.1 U/kg body weight) was followed by an infusion of ECT or saline alone. Plasma Prl peaks after hypoglycaemic stress were significantly lower in ECT-infused subjects than those in saline-injected controls (ECT, 16.5 ± 3.1 vs 33.5 ± 9.6 ng/ml, P < 0.05). In patients with prolactinoma, basal levels of plasma Prl ranging from 42.0–4130 ng/ml failed to change during iv infusion of ECT. Moreover, ECT (10−9–10−6m) did not affect Prl release from prolactinoma tissues perifused in vitro. These findings suggest that ECT may not act directly on the pituitary to modify Prl release. Rather, peripherally administered ECT appears to suppress Prl release via the central nervous system.

Ontogeny of Angiotensin-II-Induced Prolactin Release in vivo and in vitro in Female and Male Rats

1994 ◽  
Vol 59 (1) ◽  
pp. 57-62 ◽  
Author(s):  
Graciela S. Díaz-Torga ◽  
Damasia Becú-Villalobos ◽  
Carlos Libertun
Keyword(s):  
Angiotensin Ii ◽  
Male Rats ◽  
Prolactin Release

scholarly journals Changes in prolactin secretion in the short- and long-term after adrenalectomy

2012 ◽  
Vol 56 (4) ◽  
pp. 244-249 ◽  
Author(s):  
Maria Thereza C. Laguna-Abreu ◽  
Carla Germano ◽  
Ayrton C. Moreira ◽  
José Antunes-Rodrigues ◽  
Lucila Elias ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Plasma Corticosterone ◽  
Prolactin Secretion ◽  
Plasma Prolactin ◽  
Peptidergic Neurons ◽  
Prolactin Release ◽  
Short And Long Term ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
Pituitary Adrenal Axis

OBJECTIVE: To evaluate the modulation of the hypothalamus-pituitary-adrenal axis (HPA) on prolactin secretion in rats after adrenalectomy (ADX). MATERIALS AND METHODS: Plasma corticosterone, ACTH, and prolactin concentrations were measured by radioimmunoassay in rats after bilateral ADX in the short- (3 hours and 1day) and long-term (3, 7, and 14 days). RESULTS: Animals that underwent ADX showed undetectable corticosterone levels and a triphasic ACTH response with a transient increase (3h), a decrease (1d), and further increase in the long-term after ADX. Sham animals showed a marked increase in corticosterone and ACTH levels three hours after surgery, with a decrease to basal levels thereafter. Plasma prolactin levels were not changed after ADX. CONCLUSION: There are different points of equilibrium in the HPA axis after the glucocorticoid negative feedback is removed. Prolactin plasma secretion is not altered in the short or long- term after ADX, suggesting that the peptidergic neurons essential for prolactin release are not activated after ADX.

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