Prolactin-releasing peptide in the ewe: cDNA cloning, mRNA distribution and effects on prolactin secretion in vitro and in vivo

Abstract

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 characterised 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 hypothalamus. 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 concentrations. In conclusion, these results suggest that PrRP is unlikely to be an important prolactin-releasing factor in this species.

Central Administration of Neuropeptide B, But not Prolactin-Releasing Peptide, Stimulates Cortisol Secretion in Sheep

“…result, since the amino acid sequence of PrRP is identical between cattle and sheep [32]. The use of OVX ewes also does not explain this result, since it has been demonstrated that the cortisol response to stress is higher in the OVX ewe than in the estradiol-treated OVX ewe [33].…”

“…Consequently, the present result suggests that central PrRP does not participate in control of the HPA axis in sheep. Curlewis et al [32] found that PrRP mRNA is abundantly expressed in the ventromedial hypothalamus and brainstem of sheep. However, they also failed to observe any change in the plasma prolactin concentration after an icv injection of 50 nmol of PrRP in sheep [32].…”

Identification of salsolinol in the mediobasal hypothalamus of lactating ewes and its relation to suckling-induced prolactin and GH release

“…Maintenance of increased lactotroph activity during lactation seems to require additional factor(s) enhancing prolactin synthesis and release. Recently, some hypothalamic compounds are thought to play the role of prolactin-releasing factor (PRF; Maruyama et al 1999, Curlewis et al 2002, Samson et al 2003 and amongst them, salsolinol that paradoxically may be produced by the inhibitory NEDA system (Mravec 2006).…”

Prolactin and the physiological regulation of its secretion. A review

“…TRH receptors have been identified on type II and type III of lactotrophs but not any labelling was evident on type I. Other studies have revealed that the stimulatory influence of PrRPs-31 on PRL release in rats is rather low compared to TRH or VIP (Samson et al, 1998;Curlewis et al, 2002;Swinnen et al, 2005;Christian et al, 2007).…”

“…The PrRPs-31 has no stimulatory effect on PRL release in sheep (Curlewis et al, 2002), but it is essential for secretion of this hormone in teleost fish (Sakamoto et al, 2003). Chicken PrRPs-31/32 increases plasma PRL concentration in chicks when administered peripherally whereas infused centrally decreases PRL release, suggesting that in these animals PrRPs-31/32 has distinct effect on PRL secretion between tissue (Tachibana et al, 2011).…”