Prolactin modulates luteal regression from the coeliac ganglion via the superior ovarian nerve in the late-pregnant rat
Sandra S. Vallcaneras A D , Magalí de la Vega A D , Silvia M. Delgado A , Alicia Motta B , Carlos Telleria C , Ana M. Rastrilla A and Marilina Casais A D EA Laboratorio de Biología de la Reproducción (LABIR), Facultad de Química, Bioquímica y Farmacia, Universidad Nacional de San Luis, Ejército de los Andes 950 (5700) San Luis, Argentina.
B Laboratorio de Fisiopatología Ovárica. Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Paraguay 2155 (1121) Buenos Aires, Argentina.
C Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, 414 E. Clark St., Vermillion, SD 57069, USA.
D Instituto Multidisciplinario de Investigaciones Biológicas de San Luis (IMIBIO-SL), CONICET, Chacabuco 917 (5700) San Luis, Argentina.
E Corresponding author. Email: mcasais@unsl.edu.ar
Reproduction, Fertility and Development 28(5) 565-573 https://doi.org/10.1071/RD14184
Submitted: 31 May 2014 Accepted: 10 August 2014 Published: 2 September 2014
Abstract
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.
Additional keywords: nitric oxide, ovary, peripheral neural system, progesterone, prostaglandin F2 alpha.
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