The purpose of the present work was to investigate whether the administration of a dopamine agonist (2-bromo-α-ergocryptine) was able to interfere with the normal change in uterine sensitivity to oestrogen that occurs around the onset of puberty in the rat.

To determine the change in uterine sensitivity groups of rats at 25, 30 or 35 days of age were killed (to find the initial uterine weight) or ovariectomized with or without oestrogen replacement therapy (0·05 μg/100 g body wt, daily for 5 days) and then killed to determine the final uterine weight. Comparisons were made between initial and final uterine weights. Five days before the animals reached 25, 30 or 35 days of age, one group was injected with 2-bromo-α-ergocryptine (0·5 mg/100 g body wt daily for 5 days) and another one with solvent (control rats). At the ages specified (25, 30 and 35 days of age) both groups were subjected to the ovariectomy schedule. Results showed that the bromocriptine treatment was effective in blocking the normal uterine change in sensitivity that occurs at 30 days of age. At 35 days of age the dopamine agonist was able to counteract the action of oestrogen in maintaining the uterine weight 5 days after ovariectomy. The results are interpreted as suggesting that the mechanism of change in uterine responsiveness to oestrogen in maturing rats is mediated by prolactin.

Abstract

The antiprogesterone RU486 injected on the morning of pro-oestrus blunts the preovulatory secretion of LH and FSH and abolishes the secondary secretion of FSH during oestrus without affecting ovulation in the rat. To ascertain whether the secretion of LHRH is involved in these effects, we studied the effects of RU486 (4 mg/0·2 ml oil), given s.c. at 0800 h on pro-oestrus, on LHRH secretion into the pituitary stalk blood vessels and on peripheral plasma concentrations of LH and FSH at 1800 h on pro-oestrus and 0200 h on oestrus. Furthermore, we determined the effects of an s.c. injection of 1 mg of an LHRH antagonist (LHRH-A; ORG30276) at 2000 h on pro-oestrus and those of an i.p. injection of 100 ng LHRH (Peninsula 7201) at 0100 h on oestrus on serum concentrations of LH, FSH and oestradiol at 0200 h on oestrus in oil- and RU486-treated rats.

RU486 decreased LHRH secretion at 1800 h on prooestrus while this was increased at 0200 h on oestrus. While the reduction of preovulatory LHRH secretion in RU486-treated rats coincided with a reduction in both LH and FSH surges during the evening of pro-oestrus, the increased LHRH secretion during the early hours of oestrus was only accompanied by an increased concentration of LH. An injection of LHRH stimulated, while that of LHRH-A inhibited serum concentrations of LH at 0200 h on oestrus in both oil- and RU486-treated rats. An injection of LHRH-A had no effect on FSH concentration at 0200 h on oestrus in either oil- or RU486-treated rats. On the contrary, exogenous LHRH increased FSH concentration at 0200 h on oestrus only in oil-treated rats.

The results indicate that, in the rat, progesterone secretion during the afternoon and evening of pro-oestrus enhances preovulatory LHRH and suppresses LHRH release during early oestrus into the pituitary stalk blood vessels on the afternoon of pro-oestrus and during early oestrus respectively. While the secretion of LH during early oestrus is blunted by progesterone and entirely coupled to LHRH secretion, the secondary secretion of FSH during oestrus is not dependent on endogenous LHRH and at the same time is completely dependent on the actions (direct and/or indirect) of progesterone.

Journal of Endocrinology (1994) 141, 7–14

A 4×4 Latin square design in which varied doses (0, 0.5, 1.0, and 1.5 mg/kg) of 5-hydroxy-l-tryptophan (5-HTP, a serotonin precursor) were intravenously infused into late-lactation, non-pregnant Holstein dairy cows was used to determine the effects of serotonin on calcium and energy metabolism. Infusion periods lasted 4 days, with a 5-day washout between periods. Cows were infused at a constant rate for 1 h each day. Blood was collected pre- and 5, 10, 30, 60, 90, and 120 min post-infusion, urine was collected pre- and post-infusion, and milk was collected daily. All of the 5-HTP doses increased systemic serotonin as compared to the 0 mg/kg dose, and the 1.0 and 1.5 mg/kg doses increased circulating glucose and non-esterified fatty acids (NEFA) and decreased beta-hydroxybutyrate (βHBA) concentrations. Treatment of cows with either 1.0 or 1.5 mg/kg 5-HTP doses decreased urine calcium elimination, and the 1.5 mg/kg dose increased milk calcium concentrations. No differences were detected in the heart rates, respiration rates, or body temperatures of the cows; however, manure scores and defecation frequency were affected. Indeed, cows that received 5-HTP defecated more, and the consistency of their manure was softer. Treatment of late-lactation dairy cows with 5-HTP improved energy metabolism, decreased loss of calcium into urine, and increased calcium secretion into milk. Further research should target the effects of increasing serotonin during the transition period to determine any benefits for post-parturient calcium and glucose metabolism.