No abstract

No abstract

Our objective was to test the hypothesis that short-term (8 days) treatment of prepubertal heifers with melengestrol acetate (MGA) and subsequent steroid withdrawal would stimulate LH secretion and follicular growth. Angus heifers were divided randomly into two groups; MGA-treated (n = 8) or control (CON; n = 9). Puberty was determined by monitoring circulating concentrations of progesterone and ovarian morphology during a 14-day period following MGA withdrawal. LH secretory patterns were assessed upon initiation of MGA (Day 0), during MGA (Day 7), and 1 day after withdrawal of MGA (Day 9). All MGA-treated heifers, versus four CON heifers, exhibited corpora lutea and luteal phase concentrations of progesterone within 10 days after treatment (p = 0.01). Mean LH and LH pulse frequency increased (p = 0.005 and 0.0001, respectively) between Days 0 and 9 in MGA-treated heifers. In CON heifers, mean LH concentrations and pulse frequencies did not change. During the same period, diameter of the largest follicle increased in MGA-treated animals (p = 0.003) but did not change in the CON heifers. On the basis of these results, we suggest that MGA withdrawal enhances onset of puberty by stimulating pulsatile LH secretion that accelerates follicle growth to the preovulatory stage.

We tested the hypothesis that melengestrol acetate (MGA), an orally active progestin, blocks estrus and the preovulatory surge of luteinizing hormone (LH) in beef heifers. Cycling yearling Angus heifers were divided randomly into two groups: MGA-treated (n = 6) and control (n = 5). All heifers received injections of prostaglandin F2alpha (PGF) on d -25, -11, and 0 to synchronize estrus. Following the last PGF injection on d 0, heifers were fed either 0.5 mg MGA in a carrier or the MGA carrier each day for 8 d. At 4-h intervals on d 1 through 6, all heifers were observed for expression of estrous behavior, and blood samples were collected and assayed for LH. Daily blood samples were collected at 0800 on d 1 through 10 and assayed for circulating progesterone concentrations. All control heifers exhibited estrus and a preovulatory surge of LH. In each case, this was followed by increases in circulating concentrations of progesterone indicative of ovulation and normal luteal function. In contrast, none of the MGA-treated heifers exhibited estrus, LH surges, or evidence of ovulation. The results of this experiment show that MGA prevents ovulation in cattle by inhibiting the preovulatory surge of LH.

This review focuses on the role of oestrogen in male sexual behaviour using oestrogen receptor alpha and beta knockout (ERalphaKO and ERbetaKO) mouse models. ERbetaKO mice are capable of mating and producing offspring, whereas ERalphaKO mice are unable to do either. When ERalphaKO males are treated with testosterone or dihydrotestosterone (DHT), < 50% display mounting behaviour, few intromit and none ejaculate. However, concurrent treatment with testosterone and a dopamine agonist instates masculine sexual behaviour in both male and female ERalphaKO mice. Dopamine content in the preoptic area and associated regions is not affected by oestrogen receptor alpha gene disruption. However, expression of neuronal nitric oxide synthase immunoreactivity is severely reduced in ERalphaKO males compared with wild-type males. These findings, together with studies conducted in aromatase knockout mice, are at odds with the dogma that oestrogen is required during development for expression of male sexual behaviour in adults. However, they do support a role for oestrogens, mediated by oestrogen receptor alpha, in regulation and production of neuronal nitric oxide synthase, which in turn may control dopamine agonist release. As has been shown in male rats, in mice dopamine agonist release is likely to be an essential component of the neural pathway that mediates male sexual behaviour.