Role of Oxytocin in Prolactin Secretion during Late Pregnancy

Abstract

Background/Aims: During late pregnancy, the blockade of progesterone action by mifepristone (Mp) treatment induces a dopaminergic tone fall that enables naloxone (NAL) administration to release pituitary prolactin (PRL). We determined whether oxytocin (OT), which stimulates PRL secretion acting directly on anterior pituitary lactotrophs, mediates the stimulatory action of Mp and NAL on PRL secretion during late pregnancy. Methods: On day 19 of pregnancy, circulating and pituitary OT and PRL levels were measured by radioimmunoassay, 10, 20, and 30 min after NAL (given at 17:30 h) in rats pretreated with Mp (at 08:00 h). Pituitary OT receptor (OTR) expression in Mp-treated rats was evaluated by RT-PCR. Activation of OT neurons in Mp-NAL-treated rats was measured counting double immunoreactive neurons for Fos and OT (Fos-OT-ir) in supraoptic nuclei (SON), and medial (PaMM) and lateral magnocellular divisions of paraventricular nuclei. Results: Elevated serum OT and decreased pituitary OT were observed 10 min after NAL administration in both vehicle- and Mp-treated rats. This PRL increase was prevented by previous i.p. administration of an OTR antagonist, but intracerebroventricular OT administration was ineffective. Mp increased pituitary OTR expression at 18:00 h. Only Mp-NAL increased Fos-OT-ir neurons in the PaMM and SON. Conclusions: These findings suggest that PRL secretion induced by Mp-NAL treatment is preceded by OT release. These results, together with the activation of hypothalamic OT neurons and the higher expression of pituitary OTR, support the hypothesis that, during late pregnancy, OT may act at the pituitary level to facilitate PRL secretion if the inhibitory action of progesterone is blocked.

Early prognostic markers to predict unsuccessful pregnancy in dairy cattle

“…( Villegas-Gabutti et al, 2018). Oxytocin is typically linked to birth and lactation, but there is increasing evidence about its role in the events leading up to conception (Sammut et al, 2018).…”

Alterations in Hypothalamic Mechanisms Associated with Reduced Suckling-Induced Prolactin Secretion in the Lactation-Deficient OFA hr/hr Rat

“…Although in this work we have not studied the role of hypothalamic factors with stimulatory effects on PRL secretion [1], we cannot exclude that the participation of some PRL-releasing factors may be weakened or absent in OFA rats. It has been shown that oxytocin can act as a PRL-releasing factor in several reproductive situations, such as the end of pregnancy [70], lactation, pseudopregnancy, and in ovarian steroid-treated rats [71], and has a role in suckling-induced PRL secretion [71]. In OFA rats, the suckling-induced oxytocin secretion is impaired [33, 34], which could also contribute to the low circulating PRL during lactation.…”

Recent Findings on Hyperprolactinemia and its Pathological Implications: A Literature Review

“…It acts through estrogen receptors (ERs), three of which have been identified so far. These receptors include ERα, ERβ, and G protein-coupled estrogen receptor 1 (also known as G protein-coupled receptor 30); the first two are nuclear receptors and the third is a transmembrane receptor and binds to estradiol (E2) 26-28. Approximately within the distal rat PRL enhancer, there is an estrogen response element (ERE) near the monomeric Pit-1d site at about 1.5 kb upstream of the transcription initiation point.…”

“…There are also other factors that impact PRL secretion, which are not necessarily real PRL-releasing factors. For example, a dopamine antagonist has an indirect role in increasing the PRL secretion, while suckling is a real physiological state that directly leads to the increase of PRL 27 68. Other examples of these factors are VIP, galanin, PRL-releasing peptide, oxytocin, salsolinol, etc 68.…”

“…These receptors include ERα, ERβ, and G protein-coupled estrogen receptor 1 (also known as G protein-coupled receptor 30); the first two are nuclear receptors and the third is a transmembrane receptor and binds to estradiol (E2). [26][27][28] Approximately within the distal rat PRL enhancer, there is an estrogen response element (ERE) near the monomeric Pit-1d site at about 1.5 kb upstream of the transcription initiation point. In humans, the affinity of hPRL ERE for ERα, when stimulated with E2, is relatively low, but when E2 is accompanied by tumor necrosis factor-α, the affinity is elevated and transcriptional activity becomes higher.…”