The influence of acute exposure to thermal stress on the secretion of progesterone, estradiol, cortisol, and LH was monitored in 14 lactating Holstein cows. Eight cows were maintained throughout the summer in a refrigerated air-conditioned tie stall barn. An additional eight cows were maintained in outdoor corrals with access only to shade. Rectal temperatures and respiration rates of cows under heat stress conditions were elevated above the cows maintained under air conditioning. Cows in both environments exhibited similar serum concentrations of progesterone and estradiol throughout the estrous cycle. Serum cortisol concentrations were higher in heat-stressed cows compared to cows maintained under cooling. The number of LH pulses on d 5 of the estrous cycle was greatly reduced in the heat-stressed cows compared to the cows under cooling. No differences in the number of pulses of LH were observed on d 12 of the estrous cycle between cows in the two environments. Data suggest that heat stress can suppress anterior pituitary release of LH without having a measurable influence on ovarian steroid hormone secretion.

The N-methyl-N-nitrosourea (NMU) model of hormone-responsive rat mammary carcinogenesis was used to address the hypothesis that melatonin (Mel), the principle hormone of the pineal gland, inhibits tumorigenesis by acting as an anti-promoting rather than an anti-initiating agent. Daily late-afternoon injections of Mel (500 micrograms/day), restricted to the initiation phase of NMU mammary tumorigenesis, were ineffective in altering tumor growth over a 20-week period. When Mel treatment was delayed for 4 weeks after NMU and then continued through the remainder of the promotion phase, only tumor number was significantly lower than in controls. However, when Mel injections encompassed the entire promotion phase, both tumor incidence and number were significantly lower than in the controls. Although elimination of the endogenous Mel signal via pinealectomy promoted tumor growth, the effect was not statistically significant. Serum levels of estradiol and tumor estrogen receptor content were unaltered by either Mel or pinealectomy. While Mel treatment failed to affect circulating prolactin levels, pinealectomy caused a two-fold increase in serum prolactin. The estradiol-stimulated recrudescence of tumors following ovariectomy was completely blocked by either 20, 100 or 500 micrograms Mel/day or tamoxifen (20 micrograms/day). Thus, Mel appears to be an anti-promoting hormone that may antagonize the tumor-promoting actions of estradiol in this model of mammary tumorigenesis.

During the infantile period of development in the bull calf (birth to 6 weeks of age), there is a virtual absence of episodic secretion of LH. Transition from infancy to the prepubertal period (6-10 weeks of age) is characterized by the onset of episodic LH release. This study was conducted to characterize the ontogeny of episodic GnRH release during these developmental periods. During the primary experiment, calves at 2, 5, 8, and 12 weeks of age (n = 4/age) were surgically fitted with cannulae for the collection of mixed hypophyseal portal and cavernous sinus blood. Hypophyseal portal and cavernous sinus and jugular blood samples were collected over a 9- to 12-h period at 10 min intervals. No pulses of LH were observed in calves at 2 or 5 weeks of age. At 8 and 12 weeks of age, pulsatile LH release became evident with a mean of 1.0 +/- 0.3 and 2.20 +/- 0.7 pulses/10 h, respectively. Unlike LH secretion, calves at both 2 and 5 weeks of age released GnRH in a pulsatile manner (3.5 +/- 0.2 and 5.0 +/- 0.6 pulses/10 h, respectively). The frequency of pulsatile GnRH release increased from 7.9 +/- 0.4 pulses/10 h at 8 weeks of age to 8.9 +/- 0.7 pulses/10 h at 12 weeks of age. These findings demonstrate the presence of pulsatile secretion of GnRH during the infantile period of development. Furthermore, the postnatal ontogeny of pulsatile LH release in this species is associated with an increase in the frequency of pulsatile GnRH secretion.

The relationship between number of receptors for gonadotropin-releasing hormone (GnRH) and the ability of the anterior pituitary gland to release luteinizing hormone (LH) was examined in ovariectomized ewes. A GnRH antagonist was used to regulate the number of available receptors. The dose of GnRH antagonist required to saturate approximately 50 and 90% of GnRH receptors in ovariectomized ewes was determined. Thirty min after intracarotid infusion of GnRH antagonist, ewes were killed and the number of unsaturated (i.e., those available for binding) pituitary GnRH receptors was quantified. Infusion of 10 and 150 micrograms GnRH antagonist over a 5-min period reduced binding of the labeled ligand to approximately 50 and 12% of controls, respectively. The effect of reducing the number of GnRH receptors on release of LH after varying doses of the GnRH agonist, D-Ala6-GnRH-Pro9-ethylamide (D-Ala6-GnRH) was then evaluated. One of four doses of D-Ala6-GnRH (0.125, 2.5, 50 and 400 micrograms) was given i.v. to 48 ovariectomized ewes whose GnRH receptors had not been changed or were reduced to approximately 50 or 12% of control ewes. In ewes with a 50% reduction in GnRH receptors, total release of LH (area under response curve) was lower than that obtained for controls (P less than 0.01) at the 0.125-micrograms dose of D-Ala (6.1 +/- 0.7 cm2 vs. 13.5 +/- 0.7 cm2) but was not different at the 2.5-, 50- or 400-micrograms doses of D-Ala6-GnRH.(ABSTRACT TRUNCATED AT 250 WORDS)

We investigated the nature and sites of changes in the hypothalamic-pituitary axis associated with the onset of high-frequency, high-amplitude discharges of luteinizing hormone (LH) in young bulls during the transition from the infantile to the prepubertal phase of development. Blood serum and neuroendocrine tissues from bulls killed at 1, 6, 10, 14, or 18 wk of age were evaluated. Concentrations of LH in serum from bulls 1 or 6 wk old averaged less than 0.25 ng/ml and only one episodic discharge of LH was detected for 10 bulls. At 10, 14, or 18 wk, 14 of 15 bulls had episodic discharges of LH. Concentrations of testosterone in serum were progressively higher at 10, 14, and 18 wk, but the concentration of estradiol was maximal at 6 wk. The concentrations of gonadotropin-releasing hormone (GnRH) in the anterior hypothalamus, posterior hypothalamus, or median eminence were not influenced by age. However, concentration of GnRH receptors in the anterior pituitary gland increased 314% between 6 and 10 wk and the concentration of LH increased 67%. Between 6 and 10 wk, concentrations of estradiol receptors in the anterior and posterior hypothalamus declined by 68% and 46%, but the concentration of estradiol receptors in the anterior pituitary gland increased by 103%. For most characteristics, there was no major change between 10 and 18 wk. We postulate that between 6 and 10 wk of age, there is 1) removal of an estradiol-mediated block of GnRH secretion and 2) an estradiol-mediated, and possibly GnRH-mediated, increase in pituitary GnRH receptors. Together, these changes result in greatly increased stimulation of the anterior pituitary gland by GnRH between 6 and 10 wk of age and stimulation of the discharges of LH characteristic of bulls in the early prepubertal phase of development.