Injections Of Ovine Prolactin Research Articles

Prolactin Regulation of Gonadotropin-Releasing Hormone Neurons to Suppress Luteinizing Hormone Secretion in Mice

Hyperprolactinemia causes infertility, but the mechanisms involved are not known. The present study aimed to determine whether and how prolactin may influence LH secretion in the adult female mouse. Using ovariectomized, estrogen-treated (OVX+E) mice, we found that 7 d of intracerebroventricular prolactin potently suppressed serum LH levels (P < 0.05). To examine whether this central action of prolactin may involve the GnRH neurons, the effects of acute and chronic prolactin on cAMP response element-binding protein phosphorylation (pCREB) in GnRH neurons were examined using dual-label immunocytochemistry. In diestrous and OVX+E mice, a single sc injection of ovine prolactin resulted in a significant (P < 0.05) doubling of the number of GnRH neurons expressing pCREB. OVX+E mice treated with five injections of ovine prolactin over 48 h showed a 4-fold increase in the number of GnRH neurons with pCREB. To determine whether GnRH neurons might be regulated directly by prolactin, we examined prolactin receptor (PRL-R) mRNA expression in green fluorescent protein-tagged GnRH neurons by single-cell RT-PCR. As a positive control, PRL-R mRNA was measured in arcuate dopaminergic neurons obtained from green fluorescent protein-tagged tyrosine hydroxylase neurons. Three of 23 GnRH neurons (13%) were identified to express PRL-R transcripts, whereas nine of 11 arcuate dopaminergic neurons (82%) were found to coexpress PRL-R mRNA. These data demonstrate that prolactin suppresses LH levels in the mouse, as it does in other species, and indicate that it acts centrally to regulate intracellular signaling within GnRH neurons. This is likely to occur, at least in part, through the direct regulation of a subpopulation of GnRH neurons.

Prolactin acts centrally to enhance newt courtship behavior

The effects of intracerebroventricular (ICV) and intraperitoneal (IP) injections of ovine prolactin (PRL), antiserum against newt PRL, and antibody against the newt PRL receptor on the expression of courtship behavior of male newts, Cynops pyrrhogaster, were studied to see whether PRL acts centrally or peripherally to induce the behavior. Injections of PRL by either route into gonadotropin-primed males enhanced the expression of the behavior dose-dependently. The minimum effective amount of ovine PRL administered intracerebroventricularly was 0.1 μg, whereas it was 100 μg when injected intraperitoneally. ICV injection of antiserum against newt PRL blocked the spontaneously occurring male courtship behavior when the anti-newt PRL serum was given either intracerebroventricularly or intraperitoneally. The minimum effective dose of the antiserum administered intracerebroventricularly was 0.05 μl, whereas it was 20 μl when injected intraperitoneally. Neither ICV nor IP injection of preimmune serum affected the expression of the behavior. Furthermore, ICV, but not IP, administration of 0.3 μg of anti-newt PRL receptor antibody, purified from antiserum against newt PRL receptor by use of an antigen-conjugated affinity column, blocked the spontaneously occurring courtship behavior in sexually developed males. Neither ICV nor IP injection of the same amount of normal rabbit IgG affected the expression of the behavior. The results strongly suggest that endogenous PRL enhances the behavior by acting centrally through the PRL receptors localized in the brain area.

Growth hormone-releasing hormone-producing and dopaminergic neurones in the mouse arcuate nucleus are independently regulated populations.

Differentiation of hypophysiotropic neurones that regulate the secretion of growth hormone (GH) and prolactin is influenced by GH and prolactin. Genetic GH and prolactin deficiency in mutant rodent models such as the Ames dwarf (df/df) mouse results in an increase in the number of GH-stimulatory GH-releasing hormone (GHRH) neurones and a reduction of prolactin-inhibitory tuberoinfundibular dopaminergic (TIDA) neurones in the arcuate nucleus during postnatal development. The present study tested the hypothesis that these concomitant changes in numbers of tyrosine hydroxylase (TH)- and GHRH-immunoreactive neurones in df/df hypothalamus might represent a neuronal population of fixed number that undergoes a partial change in phenotype during postnatal development. To evaluate this possibility, the postnatal reduction of the df/df TIDA population was prevented by administering prolactin neonatally to preserve TH phenotype; dwarf and normal sibling mice were treated with daily injections of ovine prolactin or vehicle starting at postnatal day 12 and continuing for 30 days. Following this treatment, numbers of arcuate neurones containing GHRH or TH, or both, were quantified using immunocytochemistry. It was hypothesized that prolactin preservation of TH-immunoreactive cell number would be accompanied by either a decrease in the GHRH-producing population or an increase in numbers of cells producing both TH and GHRH. In prolactin-treated normal (DF/df) mice, numbers of arcuate TH-immunoreactive neurones were similar to those in vehicle-treated normals. Numbers of TH-positive neurones in prolactin-treated dwarfs were higher than in vehicle-treated dwarfs, and did not differ from numbers in DF/df. Numbers of GHRH-immunoreactive cells in vehicle-treated df/df were higher than in vehicle-treated DF/df, and were not different in prolactin-treated groups of either dwarf or normal mice. Neurones containing both TH and GHRH constituted 15% of the TH population, and 76% of the GHRH population, in control normal mice; in control dwarfs, double-labelled cells were 9.3% of TH and 9.9% of GHRH. Numbers of cells immunoreactive for both TH and GHRH were not affected by prolactin treatment in either mouse type. These results demonstrate that the increase in number of GHRH-expressing neurones in the df/df arcuate nucleus does not occur at the expense of the TH phenotype, and that this increase is not influenced by prolactin feedback. Although coexpression of TH and GHRH in a subpopulation indicates that TIDA and GHRH populations are not exclusive, they appear to be influenced independently by prolactin and GH signals during development.

Role of the Ventromedial Hypothalamus in Prolactin-Induced Hyperphagia in Ring Doves

Prolactin (PRL) strongly stimulates feeding activity and body weight gain in ring doves, and of the brain loci tested to date, the ventromedial hypothalamus (VMH) is the most effective site of PRL action in promoting these changes. To determine if the VMH is essential for this response, we examined the effects of VMN destruction on spontaneous feeding and on changes in food intake induced by intracerebroventricular (i.c.v.) injections of PRL. Male birds were selectively destroyed by radiofrequency lesions ( n = 6). A group of sham-lesioned males ( n = 6) served as controls. Lesioned birds exhibited a transient increase in food intake that peaked around the seventh postoperative day and declined to baseline levels by day 12. In contrast to this pattern, body weights of lesioned birds increased in parallel with food intake, but remained elevated throughout the 3-week postoperative period. During the peak period of hyperphagia in the lesioned group, food intake and body weight increases were two to three times greater in lesioned birds than in controls. After postoperative feed intake had stabilized, each bird received 5 daily i.c.v. injections of ovine PRL. Food intake and body weight increased dramatically in both groups in response to PRL treatment, and no group differences were observed in response to magnitude. We conclude that VMH destruction strongly perturbs feeding and body weight regulation in doves. However, VMH integrity is not essential for the expression of PRL-induced hyperphagia.

ER β MRNA expression in the developing rat forebrain

The effects of intracerebroventricular (ICV) and intraperitoneal (IP) injections of ovine prolactin (PRL), antiserum against newt PRL, and antibody against the newt PRL receptor on the expression of courtship behavior of male newts, Cynops pyrrhogaster, were studied to see whether PRL acts centrally or peripherally to induce the behavior. Injections of PRL by either route into gonadotropin-primed males enhanced the expression of the behavior dose-dependently. The minimum effective amount of ovine PRL administered intracerebroventricularly was 0.1 μg, whereas it was 100 μg when injected intraperitoneally. ICV injection of antiserum against newt PRL blocked the spontaneously occurring male courtship behavior when the anti-newt PRL serum was given either intracerebroventricularly or intraperitoneally. The minimum effective dose of the antiserum administered intracerebroventricularly was 0.05 μl, whereas it was 20 μl when injected intraperitoneally. Neither ICV nor IP injection of preimmune serum affected the expression of the behavior. Furthermore, ICV, but not IP, administration of 0.3 μg of anti-newt PRL receptor antibody, purified from antiserum against newt PRL receptor by use of an antigen-conjugated affinity column, blocked the spontaneously occurring courtship behavior in sexually developed males. Neither ICV nor IP injection of the same amount of normal rabbit IgG affected the expression of the behavior. The results strongly suggest that endogenous PRL enhances the behavior by acting centrally through the PRL receptors localized in the brain area.

Prolactin-Induced Regression of the Rat Corpus Luteum: Expression of Monocyte Chemoattractant Protein-1 and Invasion of Macrophages1

Monocyte chemoattractant protein-1 (MCP-1) is a potential mediator of the recruitment of monocytes/macrophages into the regressing corpus luteum (CL). We investigated whether the luteolytic effect of prolactin in the rat is associated with the expression of MCP-1 and an invasion of monocytes/macrophages. Ovulation was induced in immature female rats by injection of eCG (5 IU, s.c.) at 30 days of age. All rats were hypophysectomized 3 days later. Rats received injections of ovine prolactin (250 micrograms, s.c.) at 12-h intervals on Day 9, 10, and 11 posthypophysectomy; controls received injection of vehicle. Rats were killed by decapitation 24, 48, or 72 h after the first injection of prolactin or vehicle. In rats treated with prolactin, immunoreactive MCP-1 was detected in the CL at 24 h after the first injection, and a consistent level of staining was reached by 72 h with immunodetectable MCP-1 diffused throughout individual CL. The number of monocytes/macrophages in the CL (mean +/- SEM) increased significantly after prolactin treatment, from 3.1 +/- 1.8 at 24 h to 49.3 +/- 8.2 at 72 h (p < 0.05), and the number of monocytes/macrophages was different from that in control, vehicle-treated rats at 72 h (10.3 +/- 4.1; p < 24 and 72 h in prolactin-treated rats (p < 0.05). It is concluded that a potentially important component of the luteolytic effect of prolactin in the rat is the expression of MCP-1 and invasion of monocytes/macrophages into the CL.

The role of prolactin in realization of estradiol action in the uterus of ovariectomized rats

The aim of this study was to examine the role of prolactin (PRL) in promoting the effects of estradiol (E 2) on the uterus. Ovariectomized rats were given a single injection of E 2 dipropionate (10 μg/rat), along with injections of ovine prolactin (PRL; a single dose — 2.5 IU/rat), or injections of metoclopramide (a single dose — 0.5 mg/rat), or injections of bromocriptine (a single dose — 0.25 mg/rat). The effects of E 2 on the uterus were determined by measuring mitotic indexes; cell, nucleus and nucleolus volumes (morphometry), and DNA content (Feulgen's method) in luminal and glandular epithelia, endometrial stromal cells at 24, 36 and 48 h after the injection of E 2. It is revealed that at each time point after E 2 and PRL or metoclopramide treatment almost all the tested parameters were lower than those in control rats treated with E 2 and distilled water. The values obtained in all the periods after E 2 along with bromocriptine treatment were higher compared with those in E 2-treated animals. Most of the results are statistically significant ( P < 0.05−0.001). In the absence of E 2 none of the drugs used influenced the uterine parameters tested. The effect of PRL is likely to be mediated by their receptors in the uterus, and it occurs by changing the mechanism of estrogen action in the uterus. The actions of metoclopramide and bromocriptine are probably also mediated by PRL.

Migratory fat deposition in European quail: a role for prolactin?

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.

Prolactin may play a role in stimulating the equine ovry during the spring reproductive transition

Summary Plasma prolactin and follicular development increased significantly between the 2nd and 5th weeks of March. During this time, follicular diameters were highly correlated with plasma prolactin (r=.323, dr=64, p=.008). There was no significant rise in LH during the experimental period (lst week in Jan to the 5th week of March). Plasma prolactin was increased by blocking dopamine receptors (fluphenazine decanoate, 178.6 µg/kg, im, once every 21 days) or by a single injection of ovine prolactin (200 mg/mare, iv) given during the 1st week in January. Fluphenazine accelerated follicular growth when compared to control mares but did not result in early ovulation. Exogenous ovine prolactin caused growth of ovulatory size follicles within 3 days in 3 out of 5 treated mares. One of these mares went on to ovulate 9 weeks following injection of prolactin. The remaining 2 mares continued to produce waves of follicular growth and rcgression until they ovulated, coincident with the control group. The present studies suggest that when endogenous prolactin secretion is increased during anestrus either by dopamine receptor blockade or by administering exogenous prolactin, typical transitional follicular growth commences.

Effects of prolactin on chloride cells in opercular membrane of seawater-adapted tilapia

Effects of prolactin on morphology and numbers of chloride cells in the opercular membrane of seawater-adapted tilapia ( Oreochromis mossambicus) have been examined. Following five daily injections of ovine prolactin at a dose of 10 μg · g body wt −1, blood samples were taken and opercular membranes were removed and stained with a fluorescent mitochondrial dye (dimethylaminostyrylethylpyridiniumiodine), a fluorescent derivative of ouabain (anthroylouabain), and a histological stain specific for the extensive tubular system of chloride cells (zinc-osmium-iodine). Mean plasma osmolarity and sodium increased 23–24% following prolactin injection. An increase in the relative frequency of chloride cells between 20 and 180 μm 2 in cross-sectional area and a decrease in the relative frequency of chloride cells greater than 180 μm 2 were observed following prolactin injections. Average cell size decreased 46–70% and cell height decreased 26–38% following prolactin injections. There was no significant change in cell density. Anthroylouabain staining was observed in both prolactin- and saline-injected fish, and no significant effect on Na +,K +-adenosinetri-phosphatase activity was seen in either opercular membrane or gill tissue. The results demonstrate an effect of prolactin on chloride cell size and provide a morphological correlate for decreased secretory activity of chloride cells following prolactin injections.

In vivo voltammetry study of the modulatory action of prolactin on the mesolimbic dopaminergic system

The effects of an acute subcutaneous injection of ovine prolactin (PRL) or its vehicle on total motor activity and the extracellular levels of dopamine (DA), DOPAC and ascorbic acid (AA) in the nucleus accumbens were monitored simultaneously in freely behaving male rats. The neurochemical data were obtained by Differential Normal Pulse Voltammetry using electrochemically pretreated carbon fiber microelectrodes and numerical waveform analysis of the catechol peak. PRL treatment increased the extracellular levels of DA and DOPAC in the nucleus accumbens, which is consistent with previous reports using other methodologies. Furthermore, there was a concomitant decrease in the AA signals and motor activity. These findings suggest an antagonistic action of PRL on dopaminergic transmission in the mesolimbic system.

Time course and response specificity of prolactin-induced hyperphagia in ring doves.

Intracranial injections of prolactin (PRL) have been previously shown to elevate food and water intake in ring doves. In an attempt to further characterize these PRL-induced behavioral responses and the time course of PRL action, food and/or water intake were measured as frequent intervals in male doves given a single intracerebroventricular (ICV) injection of ovine PRL (44 pmoles) or vehicle under food deprivation, water deprivation, or nondeprivation conditions. PRL increased food consumption by 35-50% over baseline levels in water deprived and nondeprived doves, although response latencies (10 hr) and durations (greater than 24 hr) were considerably longer than those reported for other orexigenic peptides. Behavioral observations of nondeprived doves further revealed that PRL significantly increased total time spent feeding and average feeding bout duration. In contrast to this pattern, water intake remained unchanged in food deprived doves and was only marginally increased in nondeprived doves following PRL treatment. Collectively, these results suggest that PRL promotes a selective and long-lasting hyperphagia which may in turn augment drinking activity.

Prolactin and growth hormone stimulate food intake in ring doves

Ingestive behavior and body weight were measured in male and female ring doves given twice daily subcutaneous injections of ovine prolactin (7 mg/kg/day) or vehicle and in male doves given daily intracerebroventricular (ICV) injections of ovine prolactin at doses ranging from 0.1 to 2.0 μg/day. Changes induced by ICV administration of turkey prolactin, turkey growth hormone, ovine growth hormone, human growth hormone, and vehicle were also examined. Subcutaneous injections of ovine prolactin markedly increased food intake and body weight in both sexes. Similar effects occured in dose-related fashion in male doves given ICV injections of ovine prolactin. The three growth hormone preparations also increased feeding and body weight significantly, but turkey prolactin was ineffective in this regard. Changes in drinking generally paralleled feeding patterns but were less pronounced and may have been secondary to feeding changes. We conclude that feeding in this species is strongly stimulated by some prolactin and growth hormone preparations. However, the physiological mechanisms underlying these effects remain to be clarified.

Distribution of 3,4-dihydroxyphenylacetic acid (DOPAC) and 3,4-dihydroxyphenylglycol (DOPEG) in microdissected brain structures and the pituitary gland: metabolite changes in the median eminence in response to hyperprolactinemia and suckling.

Dopamine (DA), norepinephrine (NE), epinephrine (E), 3,4-dihydroxyphenylglycol (DOPEG) and dihydroxyphenylacetic acid (DOPAC) were determined simultaneously by a radioenzymatic, thin-layer chromatographic assay able to detect 1-10 pg of the parent compounds and 80-120 pg of their metabolites. A localization study of these compounds in 20 micro-dissected hypothalamic and limbic structures and the anterior and posterior pituitary glands of male rats was completed. DOPAC was detectable in 14 of 22 structures with the lowest DOPAC/DA ratio being found in the caudate nucleus (7.1%) and the highest in the medial aspect of the ventromedial nucleus of the hypothalamus (422.0%). There was a higher DOPAC/DA ratio in the lateral (21.5%) than in the medial (11.3%) portion of the median eminence suggesting that a greater portion of released DA in the medial median eminence enters the portal circulation. DOPEG was detectable in 6 of 22 structures with DOPEG/NE ratios ranging from 8% (interstitial nucleus of the stria terminalis, ventral aspect) to 32% (medial median eminence). A poor correlation exists between DOPAC and DA concentrations in the various brain regions while there was a stronger relationship between DOPEG and NE concentrations. Male rats were rendered hyper-prolactinemic for 48 hours with injections of ovine prolactin (oPRL) every 8 hours (4 mg/kg body weight sc). In such rats there was a suppression of endogenous rat PRL (rPRL) secretion, the DOPAC/DA ratio increased 2.2-fold in the medial (MEm) and 1.9-fold in the lateral median eminence (MEl), and the DA concentration in the anterior pituitary also increased 2.6-fold. In 10 day postpartum lactating rats, suckling produced marked increases in serum rPRL but no change in DOPAC/DA ratios in the ME or in the DA concentration in the anterior pituitary. The data reveal a wide range of DOPAC/DA ratios (7-422%) in brain regions containing cell bodies, axons and terminals of the different dopaminergic neuronal tracts in brain and pituitary. Considering the DOPAC/DA ratios in the MEm and MEl, it is suggested that a large perturbation of dopaminergic transmission produces a significant ratio change while a smaller perturbation is not detected by this index of neuronal metabolism.

Effects of photoperiod, hypophysectomy, and follicle-stimulating hormone on testicular follicle-stimulating hormone binding sites in golden hamsters.

Experiments were conducted to partially characterize and to examine the regulation of unoccupied testicular follicle-stimulating hormone (FSH) binding sites in adult golden hamsters. Testicular FSH binding sites were measured in the 1800 X gav fraction of whole testicular homogenates using iodinated bovine FSH. Binding of FSH was highly specific for FSH, located primarily in the testes, was time- and temperature-dependent, initially reversible, saturable, and consistent with a model consisting of a single class of high-affinity binding sites (range of equilibrium association constants (Ka) 2-12 X 10(10) M-1). Exposure of hamsters to a short photoperiod consisting of 5L:19D was associated with an increase in concentration (fmol/mg protein), but a reduction in total content (fmol/testes) of testicular FSH binding sites. There was no appreciable 5L:19D-associated alteration in receptor affinity (average Ka = 7.83 X 10(10) M-1). Injections of ovine prolactin (oPRL), ovine luteinizing hormone (oLH), or ovine FSH (oFSH) for 3 days into hamsters housed in 5L:19D for 12 wk had no effect on photoperiod-induced changes in testicular FSH binding sites. On Days 5 and 6 post hypophysectomy, a dramatic increase in FSH binding site concentration occurred, with but marginal effects on binding site affinity. Injections of 5 micrograms oFSH on Days 2, 3, and 4 after hypophysectomy prevented the increase in binding site concentrations measured on Day 5. Injection of a combination of 5 micrograms oFSH, 50 micrograms oPRL, and 25 micrograms oLH also reduced testicular FSH binding site concentrations in hypophysectomized hamsters, but oPRL or oLH by themselves were ineffective. The data indicate a homologous down-regulation of testicular FSH binding sites, but do not exclude the involvement of other hormones.

Circadian rhythm in the mammary gland response to prolactin

Abstract A Circadian rhythm in mammary gland response was observed in steroid primed Sprague‐Dawley rats which received daily injections of ovine prolactin for 5 days at either 0600, 1200, 1800, or 2400. Mammary gland weight (± SE) depended upon the time of day of prolactin injection; 5.97 ± 0.54 g (0600), 2.64 ± 0.46 g (1200), 2.75 ± 0.33 g (1800), 3.38 ± 0.36 g (2400). Consinor analysis of the response to prolactin data showed a highly significant 24‐h rhythm (P < 0.0001) with a mesor of 3.71 ± 0.24 g, an amplitude of 1.65 ± 0.66 g, and an acrophase of _77.95 ± 11.74 degrees (0512 ± 47 min.). The 105 female rats were ovariectomized at age 12 weeks and maintained in a room (22° C) on a 12‐h daily photoperiod (0600 to 1800). Steroid priming was produced by giving injections (i.p.) of2 μg of 17 s‐estradiol‐3‐benzoate and 6 mg of progesterone in 0.1 ml of corn oil for 20 days (0800 ‐ 0900), beginning 2 February). Prolactin (2 mg, 50 IU, in 0.25 ml of 0.9% saline) was injected (i.p.) at either 0600, 1200, 18...

Serum prolactin and luteinizing hormone levels during an induced pause in domestic fowl.

Serum prolactin (PRL) and luteinizing hormone (LH) levels were measured in White Leghorn hens induced to pause by fasting and exposure to 8L:16D photoschedule. Both PRL and LH levels declined during the fast and increased upon refeeding. Prolactin levels changed primarily in response to the fasting/refeeding component of the pause-inducing procedure, as exposure of non-fasted hens to an 8L:16D photoschedule exerted little effect on serum PRL levels. Injections of ovine prolactin during the pause-inducing procedure significantly reduced the subsequent rate of loss of primary wing feathers, suggesting that in certain physiological states, PRL may function to suppress molting.

Short-term effects of prolactin on prostatic function in rats with lisuride-induced hypoprolactinaemia.

The effects of a single injection of ovine prolactin on prostatic function were monitored in intact, intact androgenized and castrated-androgenized rats rendered hypoprolactinaemic after 7 days of treatment with a potent dopamine agonist, lisuride. Hypoprolactinaemia was associated with reductions in ventral prostate weight, polyamine levels, lateral lobe zinc and the concentration of the ventral prostate protein prostatein, but an elevation in the level of cytosolic oestradiol binding. Whether these differences attained statistical significance depended on whether the animals were intact, intact-androgenized or castrated-androgenized. With the exception of ventral prostate weight and lateral lobe zinc concentrations, a single injection of prolactin restored or reversed these changes towards control levels within 12 h, which could not be explained by an indirect effect of the hormone on adrenal or testicular function. No effects of lisuride or prolactin were observed with regard to the content of fructose in the coagulating gland or in the degree of prolactin binding to prostatic membranes.

Prolactin and calcium metabolism in pregnant ewes.

The effect of ovine prolactin on intestinal Ca absorption and placental Ca transfer was studied in pregnant ewes. Six groups of five animals bearing a single fetus were used and injected s.c. daily between days 121 and 135. The first group was given 0.1 microgram ovine prolactin/kg body wt per day, the second 0.1 microgram ovine prolactin/kg body wt per day plus 0.1 microgram 1 alpha-hydroxycholecalciferol (1 alpha-OH-D3)/kg body wt per day, the third 0.1 microgram ovine prolactin/kg body wt per day plus 0.20 units calcitonin/kg body wt per day, the fourth 2 micrograms bromocriptine/kg body wt per day, the fifth 2 micrograms bromocriptine/kg body wt per day plus 0.1 microgram ovine prolactin/kg body wt per day, and the sixth were controls injected with vehicle alone. The intestinal Ca absorption was measured on a duodenal loop tied off in vivo on day 136 and placental Ca transfer was evaluated between days 129 and 136. Ovine prolactin stimulated both intestinal Ca absorption and placental Ca transfer; these effects were further increased by 1 alpha-OH-D3. Calcitonin had no effect on ovine prolactin-stimulated intestinal Ca absorption, but blunted the influence of ovine prolactin on Ca placental transfer. Bromocriptine decreased both intestinal Ca absorption and Ca placental transfer but these effects of bromocriptine were overcome by simultaneous injection of ovine prolactin.

Effects of prolactin, adrenocorticotrophin, neurohypophysial peptides, cortisol, and androgens on some osmoregulatory parameters of the hypophysectomized catfish, Heteropneustes fossilis (Bloch)

Daily injections of ovine prolactin (PRL), cortisol acetate (FA), arginine vasotocin (AVT), and adrenocorticotrophic hormone (ACTH), at doses ranging from 0.1 to 500 mU/g, 0.2 to 25 μg/g, 0.01 to 0.02 μg/g, and 5 to 10 mU/g respectively, for 5 days elevated plasma osmolarity and plasma sodium levels in the 3-day hypophysectomized catfish, Heteropneustes fossilis maintained in tap water. PRL enhanced urine production and decreased urine osmolarity and sodium concentration. Administration of FA and AVT increased urine output as well as urine osmolarity and sodium concentration, thereby resulting in severe natriuresis. Simultaneous administration of PRL and FA to hypophysectomized catfish restored plasma osmolarity and sodium concentration to normal levels even in the presence of increased urinary salt loss. However, if the fishes were maintained in deionized water, administration of PRL and FA had no effect on plasma osmolarity or plasma sodium levels suggesting that these hormones increase plasma osmotic pressure by stimulating active uptake of salts from the external medium. Neither PRL nor AVT evoked any increase in plasma cortisol level indicating that their effects on catfish osmoregulation are not mediated through cortisol production. Isotocin, testosterone, and Δ 4-androstenedione had no effect on any of the plasmatic or urinary parameters. It is concluded that prolactin, cortisol, and AVT are the principal hormones for osmoionic homeostasis in this catfish and that they act through independent mechanisms.