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Experiments were conducted to investigate whether prolactin suppresses the corpus luteum during lactational quiescence in the Bennett's wallaby. In the first experiment, pouch young were removed from lactating wallabies (day 0) which were then treated daily for 7 days with either saline, or 8 mg domperidone or 2 mg ovine prolactin. In the saline-injected animals there was a transient peak in progesterone concentrations on day 4 and birth on day 28. The transient progesterone peak and births were significantly (P <0·01) delayed by 5 and 8 days in animals treated with domperidone and ovine prolactin respectively. In the second experiment, four groups of lactating wallabies were treated on day 0 with either 60 mg bromocriptine (groups C and D) or the vehicle (groups A and B). On days 0–6, groups B and D were injected daily with 2 mg ovine prolactin while groups A and C received the vehicle. In group C, three pouch young died 14–29 days after administration of bromocriptine, and there was a transient rise in progesterone on day 4 in all animals, indicating that bromocriptine resulted in immediate reactivation of the quiescent corpus luteum. New births occurred in two animals on day 28. In group D, which received bromocriptine followed by ovine prolactin for 7 days, all the original pouch young remained alive at the end of the experiment. Four of the animals from this group showed a transient progesterone peak on day 11, with births in two animals on days 35 and 36 indicating that the effects of bromocriptine were prevented whilst ovine prolactin was being administered. In one animal given ovine prolactin alone (group B), there was a transient progesterone peak and birth on days 12 and 35 respectively, suggesting that removal of exogenous prolactin may also act to terminate reproductive quiescence in some animals. In summary, these results support the hypothesis that prolactin suppresses the corpus luteum during lactational quiescence, and that the effects of bromocriptine are due to suppression of endogenous prolactin.

J. Endocr. (1988) 119, 405–411