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Summary.Artificially induced cessation of egg laying caused regression of the reproductive tract in hens, as well as changes in circulating concentrations of sex steroids. Hens were bled at several stages during and after artificial moult induced by fasting or overfeeding a diet low in calcium or high in zinc. Hens received a single injection of 200 i.u. of horse LH at Day 0, 7, 21, 35 and 77 (Exp. 1) or Day 0, 8, 23, 35 and 71 (Exp. 2) after start of the treatment to induce moult. Blood samples were taken before and 20, 40 and 60 min (Exp. 1) or 15, 30 and 45 min (Exp. 2) after LH injection. Hens which were fasted or given the diet high in zinc had low plasma progesterone concentrations and the response to LH was reduced or delayed. In hens fed low calcium the reduction in plasma progesterone was less pronounced and the responsiveness to LH was more or less maintained. Conversely, there was no response of oestradiol to LH in laying hens. However, oestradiol concentrations increased in moulting hens after LH injection, due to the high oestradiol secretion from the small white follicles, since all yolky follicles were atretic.

Rats were ovariectomized 2–4 h post partumand injected with oil or 100 μg oestradiol benzoate (OB). At 65 days of age, they were decapitated at various times and circadian plasma levels of prolactin, TSH and corticosterone were measured. Rats injected with OB had a significantly raised mean concentration of plasma prolactin, whereas levels of TSH and corticosterone did not differ from those of control rats. Plasma levels of corticosterone and prolactin were positively correlated both in oil-treated controls and oestrogenized rats. A small but not significant negative correlation existed between the levels of TSH and corticosterone in oil-treated control rats. This correlation became positive in rats neonatally injected with OB. Prolactin and TSH were positively correlated in oestrogenized rats but no correlation was found in control animals. It was possible to fit the diurnal variations of all hormones in oil-treated control and OB-injected rats to a significant sinusoidal curve. The acrophase for prolactin, but not for TSH and corticosterone, shifted significantly from 22·30 h in control rats to 14·69 h in oestrogenized rats. In oil-treated control rats, the acrophases of prolactin and corticosterone differed significantly by about 12 h from the TSH peak. In rats injected neonatally with OB, however, no difference between the acrophases of the hormones was seen.It was, therefore, possible that the shift in prolactin release and the high plasma levels were both mediated by mechanisms which are common to TSH and prolactin and whose increased susceptibility is oestrogen-dependent. The role of this abnormal phasing relationship between prolactin, corticosterone and TSH which occurred in the oestrogenized rats is discussed in relation to the high incidence of various spontaneous or induced tumours which occur during later life in these rats.

The influence of an intravenous injection of ovine prolactin on the liver monodeiodinase activity and serum concentrations of thyroid hormones and corticosterone was studied in Hisex embryos and chicks after hatching. An injection of 1 and 10 μg ovine prolactin into 18-day-old chick embryos increased serum concentrations of tri-iodothyronine (T3) five-and eightfold respectively after 2 h. At the same time serum concentrations of thyroxine (T4) and reverse T3(rT3) were decreased in the chick embryo, but only with 10 μg prolactin. This was accompanied by a doubling of the liver monodeiodinase activity. Serum concentrations of corticosterone, however, were not influenced by the prolactin injections. In the 5-day-old chicken, serum concentrations of T3, rT3, T4and liver T4-5′-monodeiodinase activity were not influenced by 1 or 10 μg prolactin. Serum concentrations of corticosterone after injection of 1 or 10 μg prolactin were doubled compared with controls. These results are compatible with a prolactin-induced shift from a T4-5-monodeiodination into a T4-5′-monodeiodination in the liver at the end of incubation. This effect, however, is not mediated through a prolactin-induced corticosterone release.J. Endocr.(1985) 104, 363–366

The influence of an intravenous injection of ovine prolactin on circulating levels of thyroid hormones was studied in Rhode Island Red embryos and chicks after hatching. In the chick embryo, 2 h after injection of 0·1 μg prolactin (on incubation day 19), serum tri-iodothyronine (T3) increased threefold; after 10 or 100 μg prolactin (on incubation day 18) serum T3increased 15- to 25-fold. These profound increases were not observed in chicks after hatching. Serum concentrations and thyroid content of thyroxine (T4) in embryos and chicks of all ages studied were not influenced by the prolactin injections. Maximal serum concentrations of reverse T3(rT3) were found on incubation day 18 (110·25 ± 23·36 pmol/l; 71·66 ± 15·18 pg/ml; n= 8), whereas after hatching no rT3could be detected. An injection of 10 μg prolactin on day 18 depressed serum rT3after 2 h to 5·68 ± 3·20 pmol/l (3·69 ± 2·08 pg/ml; n= 8; P<0·001); the effect of 100 μg prolactin was less pronounced. After hatching, chronic administration of prolactin resulted in decreased serum levels of T3, but not of T4, and hypertrophy of the follicles in the thyroid gland. It is concluded that prolactin plays a major role in the maturation of embryonic thyroid metabolism by changing the T4-5-monodeiodination into a T4-5′-monodeiodination. The hypertrophy of the thyroid gland observed after hatching following prolonged prolactin administration may be due to decreased negative feedback of T3on the hypophysis.

Pregnant rats were subcutaneously injected daily with 10 μg oestradiol benzoate (OB) and/or 1 mg bromocriptine starting on day 15 of gestation. After treatment with OB, but not bromocriptine, lower fetal body weight, fetal length and placental weight were observed. The administration of bromocriptine did not influence maternal plasma levels of prolactin, but fetal levels were decreased on day 22 of gestation. Oestradiol benzoate raised prolactin concentrations in maternal plasma on days 20 and 22, whereas fetal plasma levels were raised on day 22. This increase was counteracted by simultaneous administration of bromocriptine and OB, whereas impairment of fetal growth remained after treatment. A slight decline in fetal plasma levels of insulin was observed once, but thyroid content of triiodothyronine and thyroxine (T4) was decreased to a quarter and a third respectively of control levels in male and female fetuses of OB-treated rats, fetal circulating levels of T4were also depressed. Maternal and fetal plasma glucose levels were decreased. A close correlation between T4and placental or fetal weight was always present on day 22 of gestation. It was concluded that OB injected into pregnant rats will reach the fetal circulation as judged by increases in fetal plasma levels of prolactin. The observed fetal growth retardation after the OB injection was associated with thyroid deficiency, whereas plasma levels of prolactin and insulin were either not at all or only slightly altered. A direct effect of OB on placental blood flow and hence on the fetal food supply cannot, however, be excluded.

The effects of a long term partial food restriction were studied in chickens and rats. In chickens the treatment resulted in increased plasma T₄ levels while T₄ levels in rates remained unchanged. Plasma T₄ decreased in both species. In vitro hepatic outer ring deiodinating type I (ORD-I) activity was not influenced by the food restriction, suggesting that the amount of ORD-I enzyme present in the liver remained unchanged. In vitro hepatic inner ring deiodinating type III activity, on the contrary, was greatly increased in both species. This increase may contribute to the decreased circulating T₃ levels by increasing the degradation of T₃ and diverting the deiodination of T₄ to rT₃ instead of to T₃. Copyright 1995, 1999 Academic Press

Serum concentrations of arginine vasotocin (AVT), mesotocin and prolactin were determined by radioimmunoassay in Rhode Island Red chickens during and after dehydration, haemorrhage and oviposition. During dehydration increased circulating levels of AVT, mesotocin and prolactin were found. As water deprivation proceeded, marked differences were observed. After an initial rise in serum AVT, mesotocin and prolactin levels during mild and moderate dehydration, concentrations of both AVT and prolactin tended to normalize during continued water deprivation, while those of mesotocin remained high throughout the whole dehydration experiment with the highest at the end of the water-deprivation period. Removal of 5 ml blood at intervals of 10 min during six consecutive time-periods did not affect serum osmolality and circulating levels of AVT and prolactin, but slightly increased mesotocin. These results suggest an osmoregulatory role for AVT and prolactin, whereas mesotocin may be involved in volume control. Finally, 1 min after oviposition, control values of 19·5 ±3·4 pmol AVT/1 (n=9) were raised more than sevenfold to 142·9±12·5 pmol/l (n=11). Thereafter, a decline occurred with a half-life for AVT of 13 min with raised serum levels up to 31 min after oviposition. In contrast, the serum concentrations of mesotocin and prolactin remained unaffected by oviposition.J. Endocr.(1984) 102, 345–351

Summary.Injection of bromocriptine from 5 days before until 5 days after mating clearly suppressed the periovulatory prolactin surge in ewes in the anoestrous and oestrous season but did not change the litter size significantly. Progesterone, GH, TSH or thyroid hormone concentrations were not influenced by the bromocriptine treatment. The progesterone concentrations were lower during the first weeks after mating in the anoestrous season compared to the oestrous season, while there was no difference between pregnant and non-pregnant ewes. During later gestation this seasonal difference was only observed in the non-pregnant ewes. At the same time there was a clear difference between pregnancy and non-pregnancy in both seasons. The prolactin, GH and thyroid hormone values also varied significantly during gestation. Since these patterns are identical in pregnant and non-pregnant ewes, the fluctuations are due to environmental factors and not to pregnancy or altered progesterone concentrations. In the anoestrous season prolactin, GH, T4and T3levels were higher than in the breeding season, while rT3showed the opposite pattern. The TSH concentration did not differ between the two seasons. These results suggest that seasonal variations in prolactin, GH and thyroid hormones or the periovulatory prolactin surge do not affect litter size of ewes during pregnancy in the oestrous or the anoestrous season.Keywords:bromocriptine; litter size; pregnancy; season; ewe

Lambs originating from Suffolk, Milksheep and Texel crossbreeds were injected with saline, 500 μg ovine prolactin or 500 μg ovine GH within 30 min of parturition (n= 10). Birth weight was negatively correlated with plasma concentrations of reverse tri-iodothyronine (rT3) but not with thyroxine (T4), free T4(expressed as the free thyroxine index) or cortisol. At birth, T3and T4plasma concentrations were high and remained high during the 3-h observation period. After 3 h a significantly lower rT3concentration was found. The cortisol concentration at birth was also high (100–400 nmol/l) but decreased rapidly to basal values after 1 h. An injection of 500 μg prolactin after parturition did not influence the hormonal parameters studied except for rT3where, after 2 h, lower plasma concentrations were found compared with controls.Growth hormone raised T3levels from 4·80 ± 0·44 (s.e.m.) nmol/l at birth to 6·74 ± 0·42 nmol/l at 1 h after birth (P< 0·01) and to 6·51 ± 0·42 nmol/l after 2 h (P< 0·05). At both times these values were significantly (P< 0·001) different from saline-injected controls. GH decreased rT3from 6·77 ± 0·71 nmol/l at birth to 5·42 ± 0·54 nmol/l after 1 h (P< 0·05) and to 5·10 ± 0·45 nmol/l after 2 h (P< 0·01; values were also significantly different from saline controls at P< 0·05 and < 0·005 respectively). At the same time total and free T4concentrations were increased. No influence of prolactin or GH injection on plasma cortisol concentrations was seen. It is concluded that GH may play an important role in the maturation of thyroid functions during the perinatal period of lambs by increasing T4secretion and by increasing the conversion of T4to T3and decreasing the T4to rT3conversion rates.J. Endocr.(1986) 109,215–219

Plasma GH, tri-iodothyronine (T3), thyroxine (T4) and liver 5′-monodeiodination (5′-D) activity were measured in 18-day-old chick embryos injected with thyrotrophin-releasing hormone (TRH) and human pancreatic growth hormone releasing factor (hpGRF). Injections of 0·1 and 1 μg TRH and 1·5 μg hpGRF increased the concentration of plasma GH while injection of 15 μg hpGRF had no effect. Concentrations of plasma T3were raised after injection of TRH or hpGRF. Injections of TRH but not of hpGRF raised the concentration of plasma T4. The increases in concentration of plasma T3after injection of TRH or hpGRF were parallelled by increases in liver 5′-D activity. An injection of 0·25 μg T4significantly raised the concentration of T4in plasma but had no effect on plasma T3or liver 5′-D activity. It is concluded that the release of chicken GH by TRH or hpGRF is responsible for the observed increases in plasma concentration of T3and liver 5′-D activity.J. Endocr. (1988) 118,233–236

The effects of neonatally administered steroids on the sensitivity of the mammary gland to tumour induction by 7,12-dimethylbenz(a)anthracene was studied as a model for delayed (de)differentiating effects of steroid hormones. Immediately after birth male and female rats were gonadectomized and treated with testosterone, oestradiol or oil. Control animals were left intact. On day 45 all the gonadectomized animals and some of the control animals received an implant which delivered continuous low levels of oestradiol. The carcinogen was administered on day 55. The administration of an oestradiol implant, which increased prolactin levels in all animals, markedly reduced tumour incidence in intact female rats and increased tumour incidence in intact male rats. Neonatal administration of testosterone or oestradiol did not significantly influence tumour incidence, histopathology or oestradiol responsiveness in neonatally gonadectomized rats but tended to decrease tumour oestradiol-receptor levels. This lack of effect of neonatal steroids in gonadectomized animals suggests that the effects observed by other authors in intact rats are mediated by changes in gonadal secretions. It is concluded that the hormonal environment during and after tumour induction plays a major role in the development of 7,12-dimethylbenz(a)anthracene-induced mammary carcinomas.

The immunization of mice with an affinity-purified glycoprotein preparation from chicken pituitary tissue yielded several monoclonal antibodies towards the recently described glycosylated variant of chicken GH. As all these antibodies recognize the classical (non-glycosylated) GH molecule equally well, they provide a suitable tool for the development of both a specific immunoadsorbent and an assay method. This paper deals with the surprising purification power of the immunoadsorbent that was produced with one of the monoclonal antibodies. The resulting preparation was more than 99% pure as assessed by reversed phase high-performance liquid chromatography and sodium dodecyl sulphate-polyacrylamide gel electrophoresis, so that no further purification steps were needed before the determination of the amino acid sequence of the material. The efficiency of the purification protocol as determined by a homologous, monoclonal antibody-based radioimmunoassay was virtually absolute. Moreover, the affinity-purified GH preparation was a mixture representing the multiple molecular forms of pituitary chicken GH, including both oligomeres and glycosylated GH. The purified preparations were finally used to demonstrate the hepatic 5′-monodeiodinase-stimulating activity of GH in the chicken embryo (results not shown), in order to prove that the biological activity of the molecule had not been damaged by elution from the immunoadsorbent.J. Endocr. (1988) 118,381–387