The Experts below are selected from a list of 669 Experts worldwide ranked by ideXlab platform
M. E. El Halawani - One of the best experts on this subject based on the ideXlab platform.
-
Transcriptional changes in hypothalamic vasoactive intestinal peptide during a photo-induced reproductive cycle in the turkey
Journal of molecular endocrinology, 1998Co-Authors: Yupaporn Chaiseha, Z Tong, Orlan M. Youngren, M. E. El HalawaniAbstract:To characterize further vasoactive intestinal peptide (VIP) as the Prolactin-Releasing Factor in avian species, the present study examined hypothalamic VIP transcription and plasma Prolactin (PRL) levels during the turkey reproductive cycle. The contribution of transcription to hypothalamic VIP mRNA steady-state levels and VIP content in response to gonadal stimulating photoperiod was also investigated. Nuclear run-on transcription assays were performed using nuclei isolated from hypothalami. Cytoplasmic VIP mRNA levels, and VIP content in the median eminence and plasma PRL levels were determined by Northern blot analysis and radioimmunoassays respectively. The alterations in VIP transcription mirrored the changes in cytoplasmic VIP mRNA and VIP content during the reproductive stages. VIP transcription, cytoplasmic VIP mRNA level and VIP content were lowest in non-photostimulated birds, higher (P 0.05) were not observed during the transition from incubation to photorefractoriness, even though there was a sharp decline in circulating plasma PRL levels (P
-
Characterization of vasoactive intestinal peptide pituitary membrane receptors in turkey hens during different stages of reproduction.
Biology of reproduction, 1993Co-Authors: Israel Rozenboim, M. E. El HalawaniAbstract:Vasoactive intestinal peptide (VIP) is a Prolactin-Releasing Factor in turkey hens. Membranes from anterior pituitaries of turkey hens were used to characterize VIP receptors. Using HPLC-purified monoiodinated VIP, we found specific VIP receptors in the anterior pituitary glands. Binding was saturable and was time- and temperature-dependent. Scatchard analysis of competitive binding studies indicated two binding sites, a high-affinity binding site (Kd1) of 6.6 +/- 1.8 pM and maximum binding (Bmax1) of 1.52 +/- 0.2 pM, and a low-affinity binding site (Kd2) of 542 +/- 200 pM and Bmax2 of 15.8 +/- 8.0 pM. Binding of VIp to pituitary membranes was specific, as compared to other peptides of the glucagon family. The rank order of potency of the peptides tested was chicken VIP > porcine VIP > peptide histidine isoleucine > secretin > glucagon > growth hormone-Releasing Factor. Two binding sites were found in all the examined reproductive stages. The lowest binding site levels were found in nonphotostimulated and photorefractory birds, followed by photostimulated birds and layers; highest levels were found in incubating birds. Nest deprivation significantly reduced Bmax1 levels without changing hypothalamic VIP content. These results suggest the involvement of the anterior pituitary VIP receptors in the regulation of Prolactin secretion from the pituitary gland.
Sakae Kikuyama - One of the best experts on this subject based on the ideXlab platform.
-
Molecular cloning and functional characterization of a Prolactin-Releasing peptide homolog from Xenopus laevis
Peptides, 2006Co-Authors: Tatsuya Sakamoto, Kazutoshi Yamamoto, Sakae Kikuyama, Aiko Oda, Miyoko Kaneko, Akio Nishikawa, Akiyoshi Takahashi, Hiroshi Kawauchi, Kazuyoshi Tsutsui, Masaaki FujimotoAbstract:Abstract Amino acid sequences for identified Prolactin (PRL)-Releasing peptides (PrRPs) were conserved in mammals (>90%) or teleost fishes (100%), but there were considerable differences between these classes in the sequence ( Xenopus laevis prepro-PrRP, which can generate putative PrRPs, was cloned and sequenced. Sequences for the coding region showed higher identity with teleost PrRPs than mammalian homologues, but suggested the occurrence of putative PrRPs of 20 and 31 residues as in mammals. The amino acid sequence of PrRP20 was only one residue different from teleost PrRP20, but shared 70% identity with mammalian PrRP20s. In primary cultures of bullfrog ( Rana catesbeiana ) pituitary cells, Xenopus PrRPs increased Prolactin concentrations in culture medium to 130–160% of the control, but PrRPs was much less potent than thyrotropin-Releasing hormone (TRH) causing a three- to four-fold increase in Prolactin concentrations. PrRP mRNA levels in the developing Xenopus brain peak in early prometamorphosis, different from Prolactin levels. PrRP may not be a major Prolactin-Releasing Factor (PRF), at least in adult frogs, as in mammals.
-
Thyrotropin-Releasing hormone (TRH) is the major Prolactin-Releasing Factor in the bullfrog hypothalamus.
General and comparative endocrinology, 1993Co-Authors: Keisuke Nakajima, Daisuke Uchida, Makoto Sakai, Noriyuki Takahashi, Tadashi Yanagisawa, Kazutoshi Yamamoto, Sakae KikuyamaAbstract:A substance exhibiting potent activity in stimulating the release of Prolactin from bullfrog (Rana catesbeiana) pituitary in vitro was isolated from an acid extract of bullfrog hypothalami by gel-filtration chromatography (Sephadex G-15), ion-exchange chromatography (Mono-S HR 5/5), and reverse-phase high-performance liquid chromatography (TSK-gel ODS-120T). Its amino acid composition was similar to that of synthetic thyrotropin-Releasing hormone (TRH). Radioimmunoassay confirmed that the substance had TRH immunoreactivity. Moreover, it exhibited the same chromatographic behavior as that of synthetic TRH. These results clearly indicate that the isolated hypothalamic substance is TRH, and that it is the major Prolactin-Releasing Factor present in the bullfrog hypothalamus.
Peter J. Morgan - One of the best experts on this subject based on the ideXlab platform.
-
Evidence for the biosynthesis of a Prolactin-Releasing Factor from the ovine pars tuberalis, which is distinct from thyrotropin-Releasing hormone.
Journal of neuroendocrinology, 2002Co-Authors: E. Scott Graham, David G. Hazlerigg, Catriona A. Webster, Peter J. MorganAbstract:This study demonstrates the presence of two Prolactin-Releasing (PR) Factors in media conditioned by primary pars tuberalis cells prepared from dispersed pars tuberalis tissue. One Factor was identified as thyrotropin-Releasing hormone (TRH) on the basis of immunoreactivity and following purification by high-performance liquid chromatography and mass spectrometry. The origin of TRH in the pars tuberalis conditioned media was investigated by measuring the expression of glutaminyl-cyclase (QC) by in situ hybridization. QC expression was not detected in pars tuberalis-specific cells, but was relatively abundant in cells in the pars distalis and hypothalamic paraventricular nucleus. These data suggest that TRH is not synthesized by the ovine pars tuberalis and more likely originated from the hypothalamic neuronal processes from the paraventricular nucleus that terminate in the median eminence. The second component of the conditioned media PR bioactivity was insensitive to the TRH-antiserum, less than 1 kDa and was not retained by the C18 reverse-phase column. The biosynthesis of the PR bioactivity by pars tuberalis cells was investigated using cycloheximide, forskolin and melatonin. Cycloheximide reduced the level of PR bioactivity produced by the pars tuberalis cells. Melatonin inhibited the increased level of PR bioactivity stimulated by forskolin. Collectively, these data demonstrate the synthesis of at least one regulator of Prolactin secretion by ovine pars tuberalis-specific cells.
-
Production of a Prolactin Releasing Factor by the ovine pars tuberalis.
Journal of neuroendocrinology, 1996Co-Authors: David G. Hazlerigg, Michael H. Hastings, Peter J. MorganAbstract:The anterior pituitary hormone Prolactin is involved in the regulation of a wide variety of processes including mammary growth, lactation, reproduction and pelage growth (1). Correspondingly, in seasonal breeders, pronounced photoperiod-driven, seasonal changes occur in the levels of Prolactin secretion (2). These effects are thought to be mediated by the pineal hormone melatonin, which acts as a humoral indicator of photoperiod (3). Melatonin is thought to act through hypothalamic sites to control the gonadotrophic axis (4-6), but the sites through which melatonin modulates Prolactin remain to be established. One possibility is that melatonin acts at the level of the hypothalamus to modulate the release of the hypothalamic Prolactin inhibitory Factor, dopamine (7). However, recent evidence from hypothalamo-pituitary disconnection experiments performed in the ram suggests that the photoperiodic modulation of Prolactin secretion can occur independently of the hypothalamus, presumably due to direct effects of melatonin on the anterior pituitary (8). The only identified site of melatonin receptor expression within the ovine pituitary is the pars tuberalis (PT) (9), the cells of which are almost completely non-lactotrophic (10). Thus the possibility exists that Factors released by the PT regulate the activity of lactotrophs in the pars distalis (PD). We have investigated this hypothesis using a range of co-culture and medium-conditioning experiments on primary cultures of ovine PT and PD cells, and here we report that PT cells secrete an unidentified Factor that is a potent stimulus of Prolactin secretion by PD cells.
J. D. Curlewis - One of the best experts on this subject based on the ideXlab platform.
-
Prolactin-Releasing peptide in the ewe: cDNA cloning, mRNA distribution and effects on Prolactin secretion in vitro and in vivo
2015Co-Authors: J. D. Curlewis, D H L Kusters, J L Barclay, S T AndersonAbstract:RT-PCR followed by 5- and 3- rapid amplification of cDNA ends was used to clone and sequence ovine Prolactin-Releasing peptide (PrRP). The cDNA was char-acterised by short 5- and 3-untranslated regions and a GC-rich (71%) coding region. The nucleotide and deduced amino acid sequences for the coding region showed 95·6 and 94·9 % identity with bovine PrRP but the amino acid sequence of PrRP31 was conserved between these species. Northern blot analysis and RT-PCR showed that, as in the rat, the peptide was more abundantly expressed in the brainstem than the hypo-thalamus. However, in the ovine hypothalamus, PrRP mRNA expression was more widespread than in the rat, with expression detected in both rostral and caudal parts of the mediobasal hypothalamus. The effects of synthetic ovine PrRP on Prolactin secretion both in vitro and in vivo were also examined. In primary cultures of sheep pituitary cells, PrRP significantly (P<0·01) increased Prolactin concentrations in the culture medium but the response was not observed in every experiment and was only seen when pituitary glands were dispersed with collagenase rather than trypsin. PrRP was much less potent than TRH which caused a significant (P<0·01) two- to threefold increase in Prolactin concentrations in every experiment. Intravenous (10 and 50 nmol) or intracerebroventricular (10 and 50 nmol) injection of PrRP had no significant effect on either plasma Prolactin concentration or pulsatile LH secretion whereas intravenous injection of TRH (10 nmol) produced a highly significant (P<0·01) and more than sevenfold stimulation of plasma Prolactin con-centrations. In conclusion, these results suggest that PrRP is unlikely to be an important Prolactin-Releasing Factor in this species
-
Effects of pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal polypeptide (VIP) on hormone secretion from sheep pituitary cells in vitro.
Journal of neuroendocrinology, 1997Co-Authors: K. Sawangjaroen, Stephen T. Anderson, J. D. CurlewisAbstract:Although vasoactive intestinal polypeptide (VIP) is thought to be a Prolactin Releasing Factor, in vivo studies on sheep suggest that it is inactive in this species. Recent studies, based primarily on the rat, suggest that the related pituitary adenylate cyclase-activating polypeptide (PACAP) is also a hypophysiotrophic Factor but again in sheep, this peptide has no in vivo effects on hormone secretion despite being a potent activator of adenylate cyclase in vitro. This lack of response to either peptide in vivo in sheep could be due to the low concentration of peptide that reaches the pituitary gland following peripheral injection. In the present study we therefore adopted an alternative approach of evaluating in vitro effects of these peptides on GH, FSH, LH or Prolactin secretion from dispersed sheep pituitary cells. In a time-course study, PACAP (1 mu mol/l) increased GH concentrations in the culture medium between 1 and 4 h and again at 12 h but had no effect in the 6 and 24 h incubations. Prolactin, LH and FSH were not affected by PACAP. The response to various concentrations of PACAP (1 nmol/l-1 mu mol/l) were then evaluated using a 3 h incubation. Again Prolactin and LH were not affected by PACAP and there was a small increase in GH concentrations but only at high concentrations of PACAP (0.1 and 1 mu mol/l; P
György M. Nagy - One of the best experts on this subject based on the ideXlab platform.
-
Salsolinol, an antagonist of prolactoliberine, induces an increase in plasma catecholamine levels in the rat.
Autonomic Neuroscience: Basic and Clinical, 2004Co-Authors: Boris Mravec, Márton I.k. Fekete, Ibolya Bodnár, György M. Nagy, Richard KvetnanskyAbstract:It has been recently observed that salsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline), a putative endogenous Prolactin-Releasing Factor is a potent inhibitor of stress-induced release of epinephrine and norepinephrine. The Prolactin release caused by salsolinol was inhibited by 1-methyl-3,4-dihydroisoquinoline (1MeDIQ). Therefore, the aim of our present studies was to investigate the effect of 1MeDIQ on plasma catecholamine levels. It has been found that 1MeDIQ is able to induce a massive increase in plasma catecholamine levels. Pretreatment of the animals with a ganglionic blocker, chlorisondamine, could completely abolish the effect of 1MeDIQ on plasma norepinephrine, and plasma epinephrine levels were only significantly attenuated. Spinal cord transection between cervical and thoracic segments eliminated 1MeDIQ induced increase in epinephrine, whereas increase in plasma norepinephrine was not affected. Hence, this effect of 1MeDIQ on sympathoadrenal system activity is most probably mediated through the level of sympathetic ganglia or partially at more centrally located sites of the nervous system. These results suggest that elevation of plasma catecholamines is involved in the mechanism of action of 1MeDIQ inhibiting the biological effect of salsolinol.
-
Stress- as well as suckling-induced Prolactin release is blocked by a structural analogue of the putative hypophysiotrophic Prolactin-Releasing Factor, salsolinol.
Journal of neuroendocrinology, 2004Co-Authors: Ibolya Bodnár, Márton I.k. Fekete, Ferenc Fülöp, Boris Mravec, Lucia Kubovcakova, E. B. Tóth, Richard Kvetnansky, György M. NagyAbstract:Prolactin is secreted from the anterior lobe of the pituitary gland in response both to suckling and to stress. We recently observed that 1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (salsolinol), produced in the neurointermediate lobe of the pituitary gland, as well as in the medial basal hypothalamus, can selectively release Prolactin from the anterior pituitary. Therefore, it has been proposed that salsolinol is a putative endogenous Prolactin-Releasing Factor (PRF). Here, we report that one structural analogue of salsolinol, 1-methyl-3,4-dihydroisoquinoline (1MeDIQ), can block salsolinol-induced release of Prolactin, but does not affect Prolactin release in response to thyrotropin Releasing hormone (TRH), alpha-methyl-p-tyrosine (alpha MpT) (an inhibitor of tyrosine hydroxylase), domperidone (a D(2) dopamine receptor antagonist), or 5-hydroxytryptophan (5-HTP), a precursor of serotonin). 1MeDIQ profoundly inhibited suckling-, immobilization-, as well as formalin-stress induced Prolactin release without any influence on corticosterone secretion. The 1MeDIQ-induced reduction in Prolactin response to immobilization stress was dose-dependent. These results suggest that salsolinol can play a pivotal role in the regulation of Prolactin release induced by either physiological (suckling) or environmental (stress) stimuli.
