Expression of GnRH receptor in the canine corpus luteum, and luteal function following deslorelin acetate‐induced puberty delay

Contents The goals of this study were as follows: (Experiment 1) to examine the basic capability of canine corpora lutea (CL) to respond to GnRH by assessing expression of gonadotropin‐releasing hormone receptor (GnRH‐R) in luteal samples collected throughout the luteal lifespan from non‐pregnant dogs, and (Experiment 2) to investigate the effects of pre‐pubertal application of the GnRH agonist deslorelin acetate on luteal function following the first oestrus. Mature CL were collected during the mid‐luteal phase (days 30–45) from treated and control bitches. Transcript levels of several factors were determined: estrogen receptors (ESR1/ERα, ESR2/ERβ), progesterone (P4)‐receptor (PGR), prolactin receptor (PRLR), PGE2‐synthase (PTGES) and PGE2 receptors (PTGER2/EP2, PTGER4/EP4), vascular endothelial growth factor (VEGFA) and VEGF receptors (VEGFR1 and VEGFR2), cyclooxygenase 2 (COX2/PTGS2), steroidogenic acute regulatory protein (STAR) and 3β‐hydroxysteroid dehydrogenase (3βHSD). Additionally, levels of Kisspeptin 1 (Kiss1) and its receptor (KISS1‐R) were evaluated. Although generally low, GnRH‐R expression was time dependent and was elevated during early dioestrus, with a significant decrease towards luteal regression. In deslorelin‐treated and control dogs, its expression was either low or frequently below the detection limit. EP2 and VEGFR1 were higher in the treated group, which could be caused by a feedback mechanism after long‐term suppression of reproductive activity. Despite large individual variations, 3βHSD was higher in the deslorelin‐treated group. This, along with unchanged STAR expression, was apparently not mirrored in increased luteal functionality, because similar P4 levels were detected in both groups. Finally, the deslorelin‐mediated long‐term delay of puberty does not have negative carry‐over effects on subsequent ovarian functionality in bitches.