Distribution and Characterization of Immunoreactive Prolactin-Releasing Peptide (PrRP) in Rat Tissue and Plasma

Matsumoto, Hirokazu; Murakami, Yuko; Horikoshi, Yasuko; Noguchi, Jiro; Habata, Yugo; Kitada, Chieko; Hinuma, Shuji; Onda, Haruo; Fujino, Masahiko

doi:10.1006/bbrc.1999.0463

Cited by 71 publications

(50 citation statements)

References 4 publications

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“…nopositive nerve endings in the external region of the median eminence, the release site of classical hypophysiotrophic factors [18, 22, 23, 24]. …”

Section: Resultsmentioning

confidence: 99%

Prolactin-Releasing Peptides Do Not Stimulate Prolactin Release in vivo

et al. 2000

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The prolactin (PRL)-releasing activity of the novel prolactin-releasing peptides (PrRPs) was studied in vivo using male and lactating female rats. Whereas thyrotropin-releasing hormone effectively stimulated PRL and thyrotropin release as expected, PrRP in both animal models neither stimulated PRL secretion nor affected the release of other pituitary hormones. At the anterior pituitary level, in situ hybridization (ISH) histochemistry and Northern blot analysis revealed significantly higher expression levels of PrRP receptor (UHR-1) transcripts in female compared to male rats but not between lactating and nonlactating animals. By ISH, expression of UHR-1 mRNA was also detected in the intermediate lobe but not in the posterior pituitary. UHR-1 transcripts were also readily detectable in various hypothalamic brain areas whereas expression of PrRP mRNA was restricted to the ventral part of the dorsomedial hypothalamic nucleus but was not detected in neuroendocrine hypothalamic nuclei (e.g. PVN, SON). We thus assume that in the central nervous system, PrRP may likely have functions as a neuromodulator. However, together with the detailed cytochemical studies of various investigators that failed to detect PrRP-immunopositive nerve endings in the median eminence, our results strongly suggest that the hypothalamic PrRPs cannot be classified as hypophysiotrophic factors.

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“…nopositive nerve endings in the external region of the median eminence, the release site of classical hypophysiotrophic factors [18, 22, 23, 24]. …”

Section: Resultsmentioning

confidence: 99%

Prolactin-Releasing Peptides Do Not Stimulate Prolactin Release in vivo

et al. 2000

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“…On the day of the experiment, the animals were randomly injected intracerebroventricularly with anti-PrRP IgG [P2L-1C, 4.9 mg/ml, 10 l; Takeda Chemical (18)/control (heat-denatured anti-PrRP IgG)] and placed on the treadmill. The P2L-1C recognizes the COOH-terminal phenylalanine amide structure of PrRP31, which is necessary for PrRPs to interact with PrRP receptor (hGR3), and neutralizes PrRP-induced arachidonic acid metabolite release from hGR3 (21). The antibody and its volume that we used in this experiment were equivalent to those in our previous study (46).…”

Section: Methodsmentioning

confidence: 99%

Possible inhibitory role of prolactin-releasing peptide for ACTH release associated with running stress

Ohiwa¹,

Chang²,

Saito³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Exercise around the lactate threshold induces a stress response, defined as "running stress." We have previously demonstrated that running stress is associated with activation of certain regions of the brain, e.g., the paraventricular hypothalamic nucleus (PVN) and supraoptic nucleus, that are hypothesized to play an integral role in regulating stress-related responses, including ACTH release during running. Thus we investigated the role of prolactin-releasing peptide (PrRP), found in the ventrolateral medulla and the nucleus of the solitary tract, which is known to project to the PVN during running-induced ACTH release. Accumulation of c-Fos in PrRP neurons correlated with running speeds, reaching maximal levels under running stress. Intracerebroventricular injection of neutralizing anti-PrRP antibodies led to increased plasma ACTH level and blood lactate accumulation during running stress, but not during restraint stress. Exogenous intracerebroventricular administration of low doses of PrRP had the opposite effects. Therefore, our results suggest that, during running stress, PrRP-containing neurons are activated in an exercise intensity-dependent manner, and likewise the produced endogenous PrRP attenuates ACTH release and blood lactate accumulation during running stress. Here we provide a novel perspective on understanding of PrRP in the endocrine-metabolic response associated with running stress. running; norepinephrine; hypothalamic paraventricular nucleus; lactate threshold; rat EXERCISE AT AROUND LACTATE threshold (LT) produces a variety of beneficial physiological and psychological effects on our body (22,40). The LT is a work rate at which the steady state of blood lactate accumulation breaks down (44) and the plasma ACTH level begins to increase during graded running (7,17,29). Because it is well known that the ACTH release is a stress maker (27), moderate running can generate one kind of stress, termed running stress, if it persists above the LT. To date, little is known about its regulatory mechanism; however, it is important in understanding the mechanisms behind the variety of physiological effects caused by exercise around the LT.To examine the regulating mechanism underlying running stress, we established the rat treadmill running model and used it to identify anatomic activation of the parvocellular part of the hypothalamic paraventricular nucleus (pPVN) and the supraoptic nucleus (SON) during running stress (32, 39). The next step in our studies will be to identify the nuclei or neuropeptides that regulate ACTH release during running stress via pPVN and SON activation. The ventrolateral medulla (VLM) and the nucleus of the solitary tract (NTS) that project to the paraventricular nucleus (PVN) are known to play a crucial role in multiple stresses (4,37,43). Furthermore, recently we identified that the A2 noradrenergic cell group in the NTS and the A1 noradrenergic cell group in the VLM were activated in running stress (24,25).Prolactin releasing peptide (PrRP) was recently isolated as the endoge...

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“…Plasma and CSF samples were analyzed for PrRP as previously described (Matsumoto et al 1999a). Briefly, 1·5 ml plasma or CSF was acidified by adding 4% acetic acid (4·5 ml) and centrifuged at 25 000 g at 4 C for 30 min.…”

Section: Prrp Assaymentioning

confidence: 99%

“…The supernatant was applied to a Sep-Pak C-18 cartridge (Waters, Milford, MA, USA), washed with 10 ml water and then eluted with 4 ml acetic acid: ethanol:water (4:86:10). Samples were then concentrated using a vacuum centrifuge (Thermo Savant, Holbrook, NY, USA) and analyzed, using a two-site enzyme immunoassay for PrRP as described previously (Matsumoto et al 1999a). The two monoclonal antibodies used in this enzyme immunoassay detect common epitopes among rat, human and bovine PrRP20 (Matsumoto et al 1999a) and can measure PrRP in these species (S Hinuma, unpublished data).…”

Section: Prrp Assaymentioning

confidence: 99%

“…Samples were then concentrated using a vacuum centrifuge (Thermo Savant, Holbrook, NY, USA) and analyzed, using a two-site enzyme immunoassay for PrRP as described previously (Matsumoto et al 1999a). The two monoclonal antibodies used in this enzyme immunoassay detect common epitopes among rat, human and bovine PrRP20 (Matsumoto et al 1999a) and can measure PrRP in these species (S Hinuma, unpublished data). By cloning an ovine PrRP cDNA, it was confirmed that the ovine PrRP20 sequence is identical to bovine PrRP20 (S Hinuma, unpublished data).…”

Section: Prrp Assaymentioning

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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Distribution and Characterization of Immunoreactive Prolactin-Releasing Peptide (PrRP) in Rat Tissue and Plasma

Cited by 71 publications

References 4 publications

Prolactin-Releasing Peptides Do Not Stimulate Prolactin Release in vivo

Prolactin-Releasing Peptides Do Not Stimulate Prolactin Release in vivo

Possible inhibitory role of prolactin-releasing peptide for ACTH release associated with running stress

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

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