Neuromodulatory effect of GnRH from coeliac ganglion on luteal regression in the late pregnant rat

It has been shown that hypothyroidism in the rat produces a prolongation of pregnancy associated with a delay in the fall of circulating progesterone (P4) at term. The aim of the present work is to determine whether the delayed P4decline in hypothyroid mother rats is due to a retarded induction of P4degradation to 20αOH P4or to a stimulation of its synthesis, and to investigate the possible mechanisms that may underlie the altered luteal function. We determined by RIA the circulating profile of the hormones (TSH, PRL, LH, P4, PGF2α, and PGE2) involved in luteal regulation at the end of pregnancy and, by semiquantitative RT-PCR, the expression of factors involved in P4synthesis (CytP450scc, StAR, 3βHSD, PRLR) and metabolism (20αHSD, PGF2αR, iNOS and COX2). Our results show that the delay in P4decline and parturition is the resultant of retarded luteal regression, caused by a combination of decreases in luteolytic factors, mainly luteal PGF2α, iNOS mRNA expression and also circulating LH, and increased synthesis or action of luteotrophic factors, such as luteal and circulating PGE2 and circulating PRL. All these changes may be direct causes of the decreased 20αHSD mRNA and protein (measured by western blot analysis) expression, which in the presence of unchanged expression of the factors involved in P4synthesis results in elevated luteal and circulating P4that prolonged pregnancy and also may favor longer survival of the corpus luteum.

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Prolactin modulates luteal regression from the coeliac ganglion via the superior ovarian nerve in the late-pregnant rat

Reproduction Fertility and Development ◽

10.1071/rd14184 ◽

2016 ◽

Vol 28 (5) ◽

pp. 565 ◽

Cited By ~ 2

Author(s):

Sandra S. Vallcaneras ◽

Magalí de la Vega ◽

Silvia M. Delgado ◽

Alicia Motta ◽

Carlos Telleria ◽

...

Keyword(s):

Pregnant Rat ◽

Luteal Regression ◽

Luteal Function ◽

Prostaglandin F2 Alpha ◽

Superior Ovarian Nerve ◽

Polymerase Chain ◽

Oxide Synthase ◽

Experimental Group ◽

Gain Access ◽

Inducible Nitric Oxide

There is considerable evidence of the neuroendocrine control involved in luteal regression in the rat. In addition, circulating prolactin (PRL), which increases during the night before parturition, may gain access to the coeliac ganglion (CG), indirectly impacting the physiology of the ovary because of the known connection between the CG and the ovary via the superior ovarian nerve (SON). In this work we investigated in the CG–SON–ovary system and whether PRL added to the CG has an impact, indirectly via the SON, on luteal regression on Day 21 of pregnancy. The system was incubated without (control) or with PRL added to the CG. We measured the ovarian release of progesterone (P), oestradiol and prostaglandin F2 alpha (PGF2α) by radioimmunoassay, and nitrites (NO) by the Griess method. Luteal mRNA expression of 3β-hydroxysteroid dehydrogenase (3β-HSD), 20α-HSD, aromatase, inducible nitric oxide synthase (iNOS) and apoptosis regulatory factors was analysed by reverse transcription–polymerase chain reaction. P release, the expression of Bcl-2 and the Bcl-2 : Bax ratio was lower than control preparations, while the expression of 20α-HSD and the release of NO and PGF2α were higher in the experimental group. In conclusion, PRL acts at the CG and, by a neural pathway, modulates luteal function at the end of pregnancy.

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