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Abstract

The present study addresses the role of prolactin as a regulator of migratory fattening in European quail (Coturnix coturnix). Plasma prolactin levels in captive birds undergoing migratory fattening in an outdoor aviary and in the laboratory were measured by radioimmunoassay with an antibody raised against recombinant-derived chicken prolactin. No strong association between prolactin and migratory fattening was apparent, and prolactin levels were more closely related to daylength, with the highest concentrations being reached on long days. Plasma prolactin profiles were similar in intact and castrated male quail. Prolactin was secreted in a daily rhythm, with the highest concentrations occurring early in the photophase. However, when birds were food-restricted for 50 days during a migratory phase, there was no difference in fat deposition between birds food-deprived for the first half of the daily photophase compared with those deprived for the second half. Fattening was reduced in the food-restricted birds relative to ad libitum-fed controls, but there was no difference in plasma prolactin levels between the groups. Injections of ovine prolactin (4 mg/kg) significantly increased food intake and body mass of birds maintained on long days, but there were no differences in fattening between birds injected in the morning compared with those injected in the afternoon. Collectively, these results do not support a major role for prolactin in the regulation of migratory fat deposition in European quail.

Journal of Endocrinology (1995) 146, 71–79

ABSTRACT

The interactions between broody behaviour and changes in concentrations of plasma prolactin and LH were investigated in bantam hens. Adoption of newly hatched chicks caused incubating hens to leave their nests and prevented plasma prolactin decreasing as rapidly as in hens deprived of their nests and not given chicks. Further, the hens allowed to rear chicks came back into lay later (P< 0·001) than the hens not allowed chicks. Plasma prolactin decreased and plasma LH increased in hens deprived of their nests: these changes were reversed when the hens re-nested. The changes in plasma LH and prolactin in nest-deprived and re-nesting birds were not always synchronous; this was particularly clear immediately after nest deprivation when the increase in plasma LH preceded the decrease in the plasma prolactin. Readiness to incubate disappeared between 48 and 72 h after nest deprivation and corresponded with the time when plasma prolactin decreased to baseline values. Administration of ovine prolactin depressed (P<0·01) the initial increase in plasma LH after nest deprivation, but repeated administration of prolactin for up to 72 h failed to suppress plasma LH to the values found in incubating hens. Repeated administration of ovine prolactin at 5- to 8-h intervals for 72 h maintained readiness to incubate in nest-deprived hens. It is concluded that the secretion of prolactin in broody hens is facilitated by the presence of chicks and that increased concentrations of plasma prolactin maintain incubation behaviour. In incubating hens the secretion of LH and prolactin may be partly regulated independently. In addition, LH secretion may also be inhibited by increased plasma prolactin.

J. Endocr. (1988) 118, 279–286

SUMMARY

Ovine ¹²⁵I-labelled prolactin was incubated with a membrane-rich particulate fraction of mouse mammary gland and bound hormone was separated by centrifugation and washing. The experiments identified two types of binding activity: total binding and specific binding, the fraction of the total which could be displaced competitively by native prolactin but not by a number of other polypeptides. Two other lactogenic hormones, human chorionic somato-mammotrophin and human growth hormone, displaced ¹²⁵I-labelled prolactin in proportion to their known intrinsic lactogenic activities. Binding of ¹²⁵I-labelled prolactin was complete within 20 min at 4 or 37 °C. Scatchard analysis of the binding indicated an apparent dissociation constant (K_d ) of approximately 9 × 10⁻⁹ mol/l and a concentration of binding sites of 15·5 × 10⁻¹³ mol/mg particulate protein. The greatest rate of specific displacement of bound ¹²⁵I-labelled prolactin was observed at concentrations of prolactin between 50 and 250 ng/ml, a concentration range near the mid-point of the dose—response curve of casein induction in intact mammary cells. The saturating concentration of prolactin for specific binding to mammary particles was similar to that for casein induction in intact cells. The prolactin binding activity was sensitive to treatment with trypsin or heating at 70 °C, indicating its protein nature. These properties of the mammary prolactin binding activity are those required of a receptor for prolactin or other lactogens. Prolactin-specific binding activity was also found in particles from mouse liver, kidney, and midbrain and from the ovary, adrenal, and seminal vesicle of the rat. These results suggest a fairly widespread tissue distribution of the prolactin receptor, and potentially implicate prolactin in the hormonal regulation of these organs.

Reports in recent years that normal levels of human chorionic somato-mammotrophin (HCS) in cases of threatened abortion are associated with continuation of pregnancy (Genazzani, Aubert, Casoli, Fioretti & Felber, 1969; Singer, Desjardins & Friesen, 1970; Niven, Landon & Chard, 1972) have led to the suggestion that lactogenic hormones may play a role in the maintenance of pregnancy. Sheep prolactin at a concentration of 10 μg/ml has been shown to exert a marked inhibitory effect on myometrial activity in pregnant guinea-pigs (Manku & Horrobin, 1973), rats primed with oestrogen and progesterone (Horrobin, Lipton, Muiruri, Manku, Bramley & Burstyn, 1973), as well as in non-pregnant human myometrium (Mugambi, Mati, Thairu & Muriuki, 1973). In the present study we show that sheep pituitary prolactin at a dose of 40 μg/ml exerts a less inhibitory effect on pregnant rabbit myometrium than in the species quoted above.

Two parallel myometrial strips were obtained from the

SUMMARY

l-DOPA, within 30 min after administration, induced a highly significant decrease of plasma prolactin levels (phase 1) in a number of groups of rats, differing in age and/or endocrine status, apparently by direct inhibition of prolactin release from the pituitary. Three hours after administration of l-DOPA these low plasma prolactin concentrations in treated animals had increased (phase 2) and did not differ significantly from levels in control animals, indicating that the effect of l-DOPA on plasma prolactin levels is only of short duration. During this process some interesting phenomena were observed, especially in the animals treated with oestrone. The elimination rate of prolactin from plasma was very high (t½ = 2·8 min), as indicated by decreasing concentrations of the hormone during phase 1. Pituitary prolactin content did not change during phase 1, suggesting that prolactin synthesis was also stopped. Notwithstanding the high elimination rate, plasma prolactin regained initial concentrations in phase 2, suggesting release of a substantial part of the pituitary prolactin content. The latter, however, remained constant during the whole experiment (i.e. before l-DOPA administration and during phase 1 as well as phase 2).

The results suggested another working mechanism of l-DOPA in decreasing plasma prolactin levels, namely by stimulating the uptake of this hormone in the periphery. After the effect of l-DOPA had ceased, most of the prolactin from the periphery returned into the bloodstream, causing a rapid restoration of plasma prolactin levels without substantial release from the pituitary. The nature of the processes responsible for the peripheral uptake of prolactin is discussed.

SUMMARY

Perphenazine has previously been shown to stimulate prolactin secretion in intact and to a lesser degree in ovariectomized virgin female rats. The question whether the oversecretion of gonadotrophins (follicle-stimulating hormone and luteinizing hormone) occurring in ovariectomized animals interferes with the ability of the pituitary cells to secrete prolactin was investigated in sham-operated and ovariectomized rats after separate and combined treatment with methallibure (ICI-33828, a non-steroidal gonadotrophin suppressor) and perphenazine which served as a prolactin releaser. Pituitary and serum prolactin were measured simultaneously by radioimmunoassay. Serum prolactin detected at the end of 5 days' treatment with perphenazine (5 mg/kg/day, s.c.) was found to be increased (81 ng/ml) compared with controls (29 ng/ml). Similar treatment given to ovariectomized animals increased serum prolactin levels from 13·7 ng/ml to only 27 ng/ml. Although high doses of methallibure alone (20 mg/kg/day, s.c.) given to ovariectomized rats for 17 days restored prolactin secretion to the levels occurring in intact non-treated animals, a dose of 10 mg was ineffective. However, when 10 mg methallibure were given to perphenazine-treated ovariectomized rats, serum prolactin rose again to 80·1 ng/ml.

These results provide substantial evidence that, when the pituitary is secreting high amounts of gonadotrophin, its prolactin secretion is reduced and its ability to secrete prolactin after perphenazine challenge is limited. Once the gonadotrophic oversecretion is suppressed, more prolactin is secreted and the pituitary can again secrete high amounts of prolactin when challenged by perphenazine. The results show that in rats there exists an antagonism between gonadotrophin and prolactin secretion.

SUMMARY

The influence of prolactin on the assay of human menopausal gonadotrophin (HMG) and human chorionic gonadotrophin (HCG) has been studied. Various bioassay methods were used and the experiments were conducted in two independent laboratories.

In hypophysectomized immature male rats the response of the ventral lobe of the prostate to HMG was not affected by simultaneous administration of prolactin. It was concluded that, in the case of urinary extracts, prolactin did not interfere with the specificity of this test for interstitial cell stimulating hormone activity.

Valid assays of HMG by the rat uterus and mouse uterus tests could be obtained in the presence of relatively large quantities of prolactin.

When HCG was assayed by the rat uterus test and by tests depending on the enlargement of the accessory reproductive organs in male rats, simultaneous administration of prolactin did not affect the results obtained.

In immature male rats prolactin did not prevent the regression of the accessory organs which occurs after castration.

Department of Physiology, Queen's University, Kingston, Ontario, Canada K7L 3N6

(Received 20 May 1974)

It is well established that gonadal steroid hormones stimulate prolactin secretion and increase the level of prolactin in the blood (Meites, Lu, Wuttke, Welsch, Nagasawa & Quadri, 1972). Many studies of the factors affecting the level of prolactin in the blood have been performed with anaesthetized rats (Chen & Meites, 1970; Wuttke & Meites, 1970; Kalra, Fawcett, Krulich & McCann, 1973). However, since it is now reasonably well established that anaesthetic agents can change levels of prolactin in the circulation (Wakabayashi, Arimura & Schally, 1971; Ajika, Kalra, Fawcett, Krulich & McCann, 1972; Terkel, Blake & Sawyer, 1972), we decided to re-examine the effect of gonadal steroids upon plasma levels of prolactin in the unanaesthetized rat. Animals were castrated and prolactin levels were determined at three intervals with and without the administration of testosterone.

Young male rats

SUMMARY

Prolactin—thyroid interaction was analysed in the second metamorphosis of Diemictylus viridescens. Intraperitoneal injections of either 3 μg thyroxine (T₄) or 0·2 mg propylthiouracil (PTU) on alternate days failed to induce second metamorphosis in the red eft (land stage); 0·1 mg PTU inhibited prolactin-induced second metamorphosis. The effect of prolactin was facilitated by 0·1 μg T₄. However, 0·5 μg T₄ inhibited water-drive behaviour after initial stimulation of integumentary changes and water-drive. Larger doses of T₄ (1–3 μg) proved fatal to the efts when given together with 0·5–40 μg prolactin.

The results indicate that a certain optimal level of thyroid hormone is needed for the initiation of second metamorphosis. Nevertheless, prolactin—thyroid antagonism, previously reported in tadpoles, also occurs in the newt. Second metamorphosis appears to be brought about by a reversal of the low prolactin—high thyroid level of the eft phase to a high prolactin—low thyroid level.