Disease relevance of PRL

• Mammalian PRL increased body weight gain, liver weight, and adipose tissue weight in corticosterone-treated hypophysectomized chickens, but did not influence bone growth or the weights of the heart, pectoralis, thymi, or bursa [1].
• As the avian PRL stimulates mitogenesis of rat Nb2 lymphoma cells, the mechanism of direct PRL action on immune cells in mammals and birds seems to be similar [2].
• The correlation coefficient of [AVT] and [PRL] was decreased by half (to 0.32) during dehydration [3].
• Expression of biologically active recombinant-derived chicken prolactin in Escherichia coli [4].
• The hypertrophy of the thyroid gland observed after hatching following prolonged prolactin administration may be due to decreased negative feedback of T3 on the hypophysis [5].

Psychiatry related information on PRL

• Therefore, in the present study, we compared the effect of intracerebroventricular (ICV) injection of C-RFa and mammalian PrRP (mPrRP) on feeding behavior and plasma PRL, growth hormone (GH), and corticosterone (CORT) concentrations [6].
• 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 [7].
• In four out of five bantams the increase in nesting behavior was preceded by an increase in the secretion of prolactin [8].
• Some prolactin-injected chickens occasionally displayed the covering stance of maternal behavior [9].

High impact information on PRL

• Prolactin and early T-cell development in embryonic chicken [10].
• However, no competition for membrane sites was observed between nascent chains of rabbit globin and either nascent ovalbumin or prolactin [11].
• Furthermore, addition of growth hormone or prolactin to cultured cockerel hepatocyte monolayers resulted in the synthesis and secretion of a polypeptide that comigrates with authentic vitellogenin on polyacrylamide gels [12].
• Chicken PRL shows 77, 68, 67, 58, and 31% identity of amino acid sequence with whale, human, ovine, rat, and salmon PRLs, respectively [13].
• Primary structure of chicken pituitary prolactin deduced from the cDNA sequence. Conserved and specific amino acid residues in the domains of the prolactins [13].

Chemical compound and disease context of PRL

• The plasma concentrations of prolactin (PRL) and estradiol, time spent nesting, consumption of feed and water, body weight, and hematocrit were measured during egg laying, incubating, and brooding of the chicks in a Japanese strain of dwarf bantam hen, Chabo [14].
• 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 [5].
• Effect of dehydration, haemorrhage and oviposition on serum concentrations of vasotocin, mesotocin and prolactin in the chicken [7].
• During dehydration increased circulating levels of AVT, mesotocin and prolactin were found [7].
• In the present study the effects of TAM administration (1 mg/kg body weight on alternate days from 12 d of age) on testicular function, hypothalamic chicken gonadotropin-releasing hormone (cGn-RH-I), plasma luteinising hormone (LH), growth hormone (GH), prolactin (PRL) and testosterone were studied in juvenile White Leghorn cockerels [15].

Biological context of PRL

• The objective of the current research was to investigate the association of polymorphisms in the chicken PRL promoter region with egg production [16].
• Analysis of chicken genomic DNA showed that there is one copy of the prolactin gene in the genome [17].
• A cDNA library was prepared from mRNA isolated from anterior pituitary glands of incubating bantam hens, in which prolactin mRNA levels were predicted to be very high [17].
• The effects of CORT on PRL cell induction are GR dependent and involve an increase in PRL gene expression [18].
• Dual-labeling immunofluorescence indicated that the majority of PRL cells induced by CORT were not labeled with bromodeoxyuridine, suggesting that lactotrophs induced by CORT do not result from cell proliferation [18].

Anatomical context of PRL

• In support of this, stimulation of the turkey pituitary gland with VIP on ED24 resulted in a 4- and 3-fold increase in PRL and PRLR, respectively [19].
• Similarly, circulating levels of PRL also increased during this interval and were highly correlated with levels of the PRLR mRNA in both the pituitary gland and hypothalamus [19].
• The presence of truncated [(+) or (-)box 1] cPRLR transcripts in the sexually mature chicken testis suggests a complex mechanism of PRL action on gonadal function [20].
• PRL receptors in lymphocytes participate in the transduction of its regulatory signal into the intracellular enzymatic machinery including that of the nucleus, leading to the expression of some genes and to the synthesis of new proteins [2].
• In addition, data indicate that GH and PRL cells differentiate from a common stem cell [21].

Associations of PRL with chemical compounds

• Induction of a luciferase reporter driven by the PRL promoter was also delayed until 3 d of CORT treatment [18].
• Moreover, the results of this study also indicate that a drug that can selectively stimulate dopamine D2 receptors can also regulate PRL secretion and PRL mRNA in turkey pituitary cells in culture [22].
• In addition, a mammalian GnRH analog stimulated the release of PRL from the pituitary RPD incubated in either iso-osmotic (320 mosmol/l) or hyperosmotic (355 mosmol/l) medium, the latter normally inhibiting PRL release [23].
• In the second breeding cycle, changes in PRL and LH concentrations were similar to those observed in the first breeding cycle except that even greater increases in plasma LH and oestradiol concentrations were observed one week after hatching when the chicks were removed [24].
• Plasma concentrations of arginine vasotocin (AVT), prolactin (PRL), aldosterone (ALDO) and corticosterone (CS) were determined by radioimmunoassay [3].

Regulatory relationships of PRL

• VIP and PMA up-regulated PRL mRNA abundance was decreased two- to fourfold by PKC desensitization [25].
• The prolactin-stimulating effects of TRH may be mediated by cyclic AMP [26].
• Glucagon-induced hyperglycaemia suppressed the level of GH in the plasma and stimulated that of prolactin [27].
• The aim of this study was to test the hypothesis that prolactin may up- and down-regulate prolactin receptor gene expression in the anterior pituitary gland and hypothalamus respectively [28].
• Somatostatin had no effect on the basal or HE stimulated release of prolactin although it did inhibit the HE induced release of GH [29].

Other interactions of PRL

• Consistent with cellular ontogeny, TSHbeta mRNA increased steadily between e10 and e17, GH mRNA increased between e12 and e17, and PRL mRNA did not increase until e17 [30].
• A similar sequence for the expression of Pit-1 relative to GH and PRL during embryonic/fetal development has been reported for rodents [31].
• Northern blotting studies showed that the pituitary gland contains a single 860 base(s) mature PRL mRNA transcript irrespective of physiological state or VIP manipulation [32].
• This study provides the first immunocytochemical evidences for: (i) The presence of GH, SM-C/IGF-1, PRL and MIS bindings on chick embryonic tissues, and further supports their potential role as growth mediators during embryonic development [33].
• The effect of exogenous prolactin (PRL) on the weight and lipid content of the liver and abdominal adipose tissue as well as on the concentrations of total lipids and lipoprotein fractions (portomicrons, VLDL, LDL, HDL) in plasma was investigated in chickens [34].

Analytical, diagnostic and therapeutic context of PRL

• Molecular cloning and sequence analysis of putative chicken prolactin cDNA [17].
• In situ hybridization showed PRL mRNA to be localized in the cephalic lobe of the anterior pituitary gland in which most PRL cells, identified immunocytochemically, were found [32].
• Anterior pituitaries were dissociated into individual cells with trypsin, and the resulting cells were then subjected to reverse hemolytic plaque assays for PRL [35].
• To gain a better understanding of the physiological significance of the three different tLH-R isoforms, total RNA from the theca layer through follicular development after prolactin (PRL) treatment was analyzed by RT-PCR [36].
• Furthermore, previous studies using immunocytochemistry found that PRL- and GH-containing cells were located primarily in the cephalic (Cp) and caudal (Cd) lobes, respectively, of the anterior pituitary [21].

References