liraglutide and the α-MSH analog mentioned have palmitic acid attached in order to improve the pharmacokinetics of the drugs. Similarly, palmitoylation of anorexigenic neuropeptide prolactin-releasing peptide (PrRP) increased the stability and half-life of the
Martina Holubová, Lucie Hrubá, Barbora Neprašová, Zuzana Majerčíková, Zdeňka Lacinová, Jaroslav Kuneš, Lenka Maletínská and Blanka Železná
T Sakamoto, M Amano, S Hyodo, S Moriyama, A Takahashi, H Kawauchi and M Ando
–enter AKT. Endocrinology 143 11 –12. Fujii R , Fukusumi S, Hosoya M, Kawamata Y, Habata Y, Hinuma S, Sekiguchi M, Kitada C, Kurokawa T, Nishimura O et al. 1999 Tissue distribution of prolactin-releasing peptide (PrRP) and
K J Oliveira, T M Ortiga-Carvalho, A Cabanelas, M A L C Veiga, K Aoki, H Ohki-Hamazaki, K Wada, E Wada and C C Pazos-Moura
. Bombesin-like peptides have been shown to decrease TSH release in rodents and humans ( Pontiroli & Scarpignato 1986 , Pazos-Moura et al. 2003 ); however, only for NB is there compelling evidence for a physiological role. NB reduced serum TSH when
Lucia Kořínková, Martina Holubová, Barbora Neprašová, Lucie Hrubá, Veronika Pražienková, Michal Bencze, Martin Haluzík, Jaroslav Kuneš, Lenka Maletínská and Blanka Železná
decrease in food intake and an increase in energy consumption ( Schwartz et al . 1996 , Kwon et al . 2016 ). In addition, leptin action in the hypothalamus is connected with other anorexigenic neuropeptides, such as prolactin-releasing peptide (PrRP
G. Schettini, E. Landolfi, O. Meucci, T. Florio, M. Grimaldi, C. Ventra and A. Marino
The effect of adenosine and its analogue ( − )-N6-R-phenylisopropyladenosine (PIA) on both anterior pituitary adenylate cyclase activity and prolactin secretion was examined in the rat. Adenosine inhibited basal adenylate cyclase activity in a dose-dependent manner and also reduced the stimulation of the enzyme by vasoactive intestinal peptide (VIP). Likewise, in primary cultures of anterior pituitary cells, adenosine decreased prolactin secretion in both basal and VIP-stimulated conditions. In perifusion experiments, adenosine also inhibited prolactin release in both basal and TRH-stimulated conditions. PIA produced a biphasic pattern of response of basal adenylate cyclase activity, being inhibitory at low and stimulatory at high concentrations. In VIP-stimulated conditions, low concentrations of PIA inhibited both adenylate cyclase activity and prolactin release from primary cultures of pituitary cells, while no additive stimulatory effect was seen at high concentrations. Similarly, low concentrations of PIA reduced both basal and TRH-stimulated prolactin release from perifused pituitaries, while increasing PIA concentrations restored prolactin release. These data show that adenosine affects basal and stimulated prolactin secretion from anterior pituitary cells. Adenosine receptors seem to be coupled to the adenylate cyclase system in the anterior pituitary gland, suggesting a possible relationship between the effect of adenosine on adenylate cyclase activity and prolactin secretion.
T Florio and G Schettini
Somatostatin is a peptide widely distributed in both the central nervous system (CNS) and peripheral tissues. It is found as two bioactive peptides of 14 and 28 amino acids, the latter being an N-terminal-extended form (Reichlin 1983a).
The name somatostatin comes from its initial discovery as an inhibitor of growth hormone (GH) release from anterior pituitary cells (Brazeau et al. 1973). Since then, numerous other physiological activities of somatostatin have been discovered associated with differing peptide and receptor localization (Reichlin 1983a,b). Besides GH, somatostatin is also able to inhibit secretion of prolactin (PRL) and thyroid-stimulating hormone (TSH) (Reichlin 1983a). In the CNS, the highest somatostatin concentrations have been detected in the hypothalamus in the tuberoinfundibular neurons where, acting as a neurohormone, the peptide regulates the hypothalamic-hypophyseal axis (Schettini 1991). Somatostatin-containing neurons are also present in many other areas of the brain, such as the cerebral cortex,
A Scorziello, E Landolfi, M Grimaldi, O Meucci, C Ventra, A Avallone, A Postiglione and G Schettini
We studied the effect of adenosine on prolactin secretion by the anterior pituitary, and the transduction mechanisms whereby the purine exerts its action. Adenosine inhibited prolactin release in basal and in vasoactive intestinal peptide (VIP)- or TRH-stimulated conditions. Pertussis toxin pretreatment reduced the inhibition of VIP-stimulated prolactin secretion which was induced by adenosine, while it completely abolished the effect of the purine on TRH-evoked prolactin release. In membrane preparations of anterior pituitary cells, adenosine reduced the adenylate cyclase activity stimulated by VIP. Such an inhibition was not blocked by pertussis toxin pretreatment.
Furthermore, the purine reduced TRH-stimulated inositol phosphate production in cultured anterior pituitary cells, an effect that was reversed by pretreatment with pertussis toxin. In addition, the nucleoside did not significantly affect the TRH-induced rise in intracellular calcium.
In conclusion, our data show that adenosine inhibits prolactin secretion, acting on purinergic receptors coupled to the adenylate cyclase enzyme and phospholipase C. The effect of the nucleoside on adenylate cyclase seems to be achieved either by the involvement of an adenosine receptor coupled to the catalytic subunit of the enzyme via a pertussis toxin-sensitive G protein, or by the activation of a site directly coupled to the catalytic subunit of the adenylate cyclase (the P site). Its effect on phospholipase C seems to be mediated by a purinergic receptor coupled to the intracellular effector via a pertussis toxin-sensitive G protein.
Y Chaiseha, Z Tong, OM Youngren and ME El Halawani
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) in laying hens, and greatest (P<0.05) in incubating birds. These increases paralleled the changes in circulating plasma PRL levels. Changes in VIP transcription (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<0.05). Following photostimulation, VIP transcription, cytoplasmic VIP mRNA levels, and VIP content increased as the hens progressed towards sexual maturity (P<0.05), and these increases were correlated with an increased plasma PRL level. These results suggest that VIP is regulated in large part at the transcriptional level during the turkey reproductive cycle and that this transcriptional regulation is coupled to the photo-induced increase in PRL secretion.
L-J Chew, V Seah, D Murphy and D Carter
It is well established that oestrogens can stimulate prolactin (PRL) secretion as well as the expression of the vasoactive intestinal peptide (VIP) gene whose product is also a potent PRL secretagogue. Previous evidence has supported both an autocrine and a paracrine role for pituitary VIP in PRL release in vitro; however, the cellular origin of VIP in pituitary tissue still remains poorly defined. In these studies, we have demonstrated by in situ hybridisation that VIP RNA is detected in the anterior pituitaries of chronically hyperoestrogenised rats, but not in those of untreated animals. Using a double-probe labelling procedure, VIP RNA has been shown to be present in a subpopulation of PRL-producing cells, while colocalisation of VIP and GH RNA was not observed. VIP gene expression in the rat anterior pituitary gland was characterised by the presence of two alternatively polyadenylated transcripts, 1·7 kb and 1·0 kb in size. We have generated a probe specific for the 1·7 kb transcript and double-labelling studies also showed definitive colocalisation with PRL mRNA. Our results demonstrating the presence of VIP RNA in PRL-producing cells thus suggest that VIP may play an autocrine role in PRL hypersecretion under conditions of oestrogen-induced hyperplasia.
A Al Kahtane, Y Chaiseha and M El Halawani
It is well documented that prolactin (PRL) release and PRL gene expression in birds are controlled by the tonic stimulation of hypothalamic vasoactive intestinal peptide (VIP). However, there is good evidence that dopamine (DA) exerts both stimulatory (at the hypothalamic level) and inhibitory (at the pituitary level) effects on PRL secretion. The interactions between VIP and DA in the regulation of PRL gene transcription are not known. This study was designed to examine the effects of a D(2) DA receptor agonist (D(2)AG; R(-)-propylnorapomorphine HCl) on basal and VIP-stimulated PRL gene transcription rate, PRL mRNA steady-state levels, PRL mRNA stability and PRL release from cultured turkey anterior pituitary cells. The D(2)AG (10(-)(10) M) completely inhibited the stimulatory effect of VIP (10(-)(7) M) upon nascent PRL mRNA as determined utilizing a nuclear run-on transcription assay. To examine further the effect of the D(2)AG on PRL mRNA post-transcriptional events, anterior pituitary cells were treated with different concentrations of D(2)AG (10(-)(12)-10(-)(4) M). Semi-quantitative RT-PCR and RIA were performed to determine the levels of PRL mRNA and PRL content in the medium respectively. The results show that D(2)AG inhibited VIP-stimulated PRL mRNA steady-state levels as well as basal and VIP-stimulated PRL release, effects which were diminished by the D(2) DA receptor antagonist, S(-)-eticlopride HCl (10(-)(10) M). Actinomycin D (5 microg/ml), an inhibitor of mRNA synthesis, was used to assess the effect of D(2)AG on PRL mRNA stability in response to VIP. The stimulatory effect of VIP on PRL mRNA stability was completely negated by the D(2)AG (from a half-life of 53.0+/-2.3 h in VIP-treated cells to 25.5+/-1.6 h in D(2)AG+VIP-treated cells, P<or=0.05). These results support the hypothesis that VIP and DA play a major role in the regulation of PRL gene expression in avian species, at both the transcriptional and post-transcriptional levels. In addition, these findings suggest that the DAergic system inhibits PRL release and synthesis by antagonizing VIP at the pituitary level via D(2) DA receptors.