Stimulation of Prolactin Release by Prolactin-Releasing Peptide in Rats

Matsumoto, Hirokazu; Noguchi, Jiro; Horikoshi, Yasuko; Kawamata, Yuji; Kitada, Chieko; Hinuma, Shuji; Onda, Haruo; Nishimura, Osamu; Fujino, Masahiko

doi:10.1006/bbrc.1999.0789

Cited by 110 publications

(64 citation statements)

References 11 publications

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“…Only a few years ago, a specific prolactin-release promoting peptide has been identified and characterised in the hypothalamus [11,12]. In addition, several other prolactin-stimulating factors have been reported, such as serotonin [13] and thyrotrophin-releasing hormone (TRH) [14][15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

Effects of the dopamine agonist cabergoline on the pulsatile and TRH-induced secretion of prolactin, LH, and testosterone in male beagle dogs

Koch

Hoppen²,

Dieleman

et al. 2006

Theriogenology

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In the present study, the pulsatile serum profiles of prolactin, LH and testosterone were investigated in eight clinically healthy fertile male beagles of one to six years of age. Serum hormone concentrations were determined in blood samples collected at 15 min intervals over a period of 6 h before (control) and six days before the end of a four weeks treatment with the dopamine agonist cabergoline (5 mg kg À1 bodyweight/day). In addition, the effect of cabergoline administration was investigated on thyrotropin-releasing hormone (TRH)-induced changes in the serum concentrations of these hormones.In all eight dogs, the serum prolactin concentrations (mean 3.0 AE 0.3 ng ml À1 ) were on a relatively constant level not showing any pulsatility, while the secretion patterns of LH and testosterone were characterised by several hormone pulses. Cabergoline administration caused a minor but significant reduction of the mean prolactin concentration (2.9 AE 0.2 ng ml À1 , p < 0.05) and did not affect the secretion of LH (mean 4.6 AE 1.3 ng ml À1 versus 4.4 AE 1.7 ng ml À1 ) or testosterone (2.5 AE 0.9 ng ml À1 versus 2.4 AE 1.2 ng ml À1 ). Under control conditions, a significant prolactin release was induced by intravenous TRH administration (before TRH: 3.8 AE 0.9 ng ml À1 ,

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Section: Introductionmentioning

confidence: 99%

Effects of the dopamine agonist cabergoline on the pulsatile and TRH-induced secretion of prolactin, LH, and testosterone in male beagle dogs

Koch

Hoppen²,

Dieleman

et al. 2006

Theriogenology

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“…Indeed, whether PrRP plays any physiological role in the release of prolactin is unclear. Using PrRP at doses 10 4 to 10 5 times the concentration we have detected in hypophyseal portal blood, some studies on the rat have shown that PrRP is able to stimulate prolactin secretion both in vitro (Hinuma et al 1998, Tokita et al 1999, Kawamata et al 2000 and in vivo (Matsumoto et al 1999b). Indeed, treatments with 1 nM (3·6 µg) PrRP31 were ineffective in stimulating prolactin secretion from isolated rat pituitary cells (Hinuma et al 1998, Tokita et al 1999, Kawamata et al 2000.…”

Section: Discussionmentioning

confidence: 94%

“…Indeed, treatments with 1 nM (3·6 µg) PrRP31 were ineffective in stimulating prolactin secretion from isolated rat pituitary cells (Hinuma et al 1998, Tokita et al 1999, Kawamata et al 2000. Other recent studies have also implicated PrRP in the estradiol-induced prolactin surge of the rat (Matsumoto et al 1999b, Hizume et al 2000. In contrast, PrRP administered in vivo had no effect on prolactin secretion in both the rat (Jarry et al 2000) and sheep (Curlewis et al 2002).…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, PrRP administered in vivo had no effect on prolactin secretion in both the rat (Jarry et al 2000) and sheep (Curlewis et al 2002). Although an extensive network of PrRP immunoreactive fibers has been described in the rat brain (Matsumoto et al 1999b), PrRP fibers are not detected in the external zone of the median eminence (Maruyama et al 1999. Moreover, a recent study employing push-pull perfusion in the rat median eminence/arcuate nucleus region found that, at the time of the LH surge, PrRP did not increase, whereas there was a significant increase in GnRH (Watanobe 2001).…”

Section: Discussionmentioning

confidence: 99%

“…However, much controversy surrounds this peptide. Although some studies suggest that PrRP stimulates prolactin release during in vitro (Hinuma et al 1998, Samson et al 1998 and in vivo (Matsumoto et al 1999b) studies, other investigations have revealed little or no effect (Jarry et al 2000, Seal et al 2000, Curlewis et al 2002. Moreover, little or no immunoreactive PrRP has been detected in the external zone of the median eminence in the rat, suggesting that PrRP is not released into the hypophyseal portal system (Maruyama et al 1999.…”

Section: Introductionmentioning

confidence: 99%

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Prolactin release during the estradiol-induced LH surge in ewes: modulation by progesterone but no evidence for prolactin-releasing peptide involvement

Skinner¹,

Caraty²

2003

Journal of Endocrinology

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An estradiol-induced prolactin surge accompanies the LH surge in several species, including sheep. However, the neural mechanisms underlying this surge remain poorly understood. A first study on estradiol-and progesteronetreated ovariectomized ewes examined whether the prolactin surge, like the LH surge, is sensitive to progesterone. Our data clearly showed that the estradiol-induced prolactin surge in the ewe is blocked by continuous exposure to progesterone and, importantly, that this blockade is overcome by pretreatment with the progesterone receptor antagonist, RU486. In a second study, we established that the generation of the prolactin surge is not dependent on the co-secretion of a prolactin-releasing peptide in the hypophyseal portal blood or cerebrospinal fluid. The neuronal pathways targeted by estradiol and progesterone to modulate prolactin secretion at the time of the LH surge remain to be identified. Importantly, it has not been established whether there is any overlap in the neuronal systems generating the gonadotropin-releasing hormone and prolactin surges.

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The activity of prolactin releasing peptide correlates with its helicity

et al. 2013

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The prolactin releasing peptide (PrRP) is involved in regulating food intake and body weight homeostasis, but molecular details on the activation of the PrRP receptor remain unclear. C-terminal segments of PrRP with 20 (PrRP20) and 13 (PrRP8-20) amino acids, respectively, have been suggested to be fully active. The data presented herein indicate this is true for the wildtype receptor only; a 5-10-fold loss of activity was found for PrRP8-20 compared to PrRP20 at two extracellular loop mutants of the receptor. To gain insight into the secondary structure of PrRP, we used CD spectroscopy performed in TFE and SDS. Additionally, previously reported NMR data, combined with ROSETTANMR, were employed to determine the structure of amidated PrRP20. The structural ensemble agrees with the spectroscopic data for the full-length peptide, which exists in an equilibrium between α- and 310-helix. We demonstrate that PrRP8-20’s reduced propensity to form an α-helix correlates with its reduced biological activity on mutant receptors. Further, distinct amino acid replacements in PrRP significantly decrease affinity and activity but have no influence on the secondary structure of the peptide. We conclude that formation of a primarily α-helical C-terminal region of PrRP is critical for receptor activation.

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Stimulation of Prolactin Release by Prolactin-Releasing Peptide in Rats

Cited by 110 publications

References 11 publications

Effects of the dopamine agonist cabergoline on the pulsatile and TRH-induced secretion of prolactin, LH, and testosterone in male beagle dogs

Effects of the dopamine agonist cabergoline on the pulsatile and TRH-induced secretion of prolactin, LH, and testosterone in male beagle dogs

Prolactin release during the estradiol-induced LH surge in ewes: modulation by progesterone but no evidence for prolactin-releasing peptide involvement

The activity of prolactin releasing peptide correlates with its helicity

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