Roles of prolactin and the uterus in the control of luteal regression in the Bennett's wallaby (Macropus rufogriseus rufogriseus)

Abstract

The factors responsible for controlling luteal regression in macropodid marsupials are unclear. Experiments were designed to examine the role of the uterus and the pre-partum prolactin pulse in this process. In experiment 1, two groups of adult female Bennett's wallabies were hysterectomized (n = 3) or sham-hysterectomized (n = 3) on Day 16 of a non-pregnant oestrous cycle and daily peripheral blood samples were collected between Days 10-37. In both groups, circulating progesterone concentrations declined to below 0.96 nmol L-1 at luteolysis on Days 28-33. Circulating prolactin concentrations remained low over the period of luteal regression. In experiment 2, two groups of animals, which were maintained in the presence of a fertile male and synchronized by the removal of pouch young (RPY), were treated on Day 16 after RPY with a single injection of long-acting bromocriptine (Parlodel LA, Sandoz Ltd, Basle, Switzerland; 50 mg per animal n = 5) or vehicle (n = 4). Vehicle-treated animals gave birth on Day 28 (n = 3) or Day 29 (n = 1) with a significant elevation of prolactin on Day 28. In contrast, 4 of the 5 bromocriptine-treated animals failed to give birth and one gave birth on Day 29. No comparable prolactin pulse was detected in any of them. Circulating progesterone concentrations declined later in the bromocriptine-treated group than in the controls. These data suggest that different mechanisms lead to luteolysis in pregnant and non-pregnant animals; in pregnancy the luteolytic signal is prolactin, whereas in the non-pregnant cycle another signal of non-uterine origin is involved.