Courtship stimulates aromatase activity in preoptic area of brain in male ring doves.

Aromatase activity was quantified in vitro in different regions of the basal forebrain of male ring doves at various times after the initiation of courtship. By 24 h after the introduction of a female dove into the cage of a male, there was a significant, nearly two-fold, increase in aromatase activity which was confined to the ventromedial preoptic area (VM-POA) where enzyme activity was concentrated. This increase in aromatase activity, which was sustained through day 5 of courtship, presumably serves to activate nest-oriented behavior.

Effect of gonadotrophin-releasing hormone on circulating levels of immunoreactive luteinizing hormone in fetal rats.

Concentrations of luteinizing hormone (LH) were measured in plasma samples obtained from rat fetuses after injecting them with synthetic gonadotrophin-releasing hormone (GnRH) in utero. On days 17 1/2, 18 1/2 or 19 1/2 post-conception (p.c.), fetuses in one uterine horn were injected subcutaneously with 100 ng GnRH in 2 microliters of saline. Fetuses in the other uterine horn were injected with saline (four litters at each gestational age). Plasma samples were collected beginning 30 min after injection of GnRH. The concentration of LH in 20 microliters of fetal plasma was measured by a microvolume radioimmunoassay. On day 17 1/2 p.c., LH was detectable only in plasma samples of GnRH-injected fetuses. In 18 1/2- and 19 1/2-day-old fetuses LH reached detectable levels (greater than 6 ng/ml) in most saline-injected fetuses. In 18 1/2- and 19 1/2-day-old fetuses of both sexes, plasma LH titers of GnRH-injected fetuses were significantly higher than in saline-injected littermates. On day 19 1/2 GnRH-treated females had higher levels of plasma LH than similarly treated males. Thus fetal rat pituitaries were shown to have the capacity to release LH in vivo in response to circulating GnRH as early as 17 1/2 days p.c.

Responsiveness to estradiol in central nervous system of aging female rats.

The age related decline in reproductive capacity in the female rat is examined in terms of physiological and behavioral changes in responsiveness to estradiol evidenced during the second year of life. After 9-12 months of age, regular estrous cycles are replaced by constant estrous, prolonged pseudopregnancy, or anestrous states, with concurrent alterations in endocrine function. Some of the mechanisms implicated in the mediation of these changes are reviewed. Estrogenic influences on estrous behavior and the control of feeding and body weight in aged rats, as well as the effects of parity on aged endocrinological functioning are discussed.

Deficits in pituitary and brain cell nuclear retention of (3H)Estradiol in diabetic rats deprived of insulin: time course and metabolic correlates.

Withdrawal of exogenous insulin for 24 h in ovariectomized, streptozotocin-diabetic rats significantly impairs estradiol uptake in whole homogenate fractions of hypothalamus-preoptic area and pituitary gland. Significant reductions in cell nuclear fractions from the same tissues are seen after 36 h of insulin deprivation. Subsequent reinstatement of insulin treatment does not yield full recovery of estradiol uptake after 24 h of insulin replacement. Fat content of the diet has no effect on brain or pituitary estradiol uptake in diabetic animals deprived of insulin for 36 h. Circulating levels of triglycerides, ketones, glucose, glycerol and free fatty acids were found to predict uptake levels to a significant extent, but no single metabolite is reliably predictive across tissues. These data demonstrate that insulin-dependent changes in brain and pituitary uptake of estradiol in rats are slow to develop, and they support the hypothesis that at least some of the reproductive dysfunctions observed in diabetic rats may be the result of impaired cell nuclear estradiol binding in hypothalamus and pituitary.

Estrous behavior and pituitary and brain cell nuclear retention of [3H]estradiol in chronically insulin-deficient female rats.

Chronic insulin deficiency, produced by administration of 60 mg/kg streptozotocin, leads to reduced estrous behavior and lower estradiol uptake in both whole homogenate and cell nuclear fractions of hypothalamus-preoptic area and pituitary gland in ovariectomized rats. High dietary fat intake produces an ameliorative effect on both lordosis behavior and estradiol uptake, relative to animals fed a standard, carbohydrate-rich diet. Plasma glucose levels are significantly correlated with estradiol uptake levels in brain and pituitary, and with plasma radioactivity levels. The data support the hypothesis that some of the reproductive dysfunctions manifest in female diabetic rats are the result of alterations in nuclear binding of estradiol by central nervous tissue, and that chronic fuel deprivation may represent an important correlate of disruptions in normal steroid action among diabetics.

In vivo cell nuclear binding of 17 beta-[3H]estradiol in rat adipose tissues.

Rat adipose tissues contain high-affinity, hormone-specific cytoplasmic estrogen receptors. If adipose tissues are actually estrogen target tissues, then it should be possible to demonstrate in vivo binding and retention of 17 beta-[2H]estradiol in adipose tissue cell nuclei, the putative subcellular site of steroid action. Gonadectomized rats were given an intravenous injection of 40 microCi (0.11 microgram) 17 beta-[2,4,6,7-3H]estradiol. Animals were then killed, and cell nuclei were isolated from hypothalamus and various fat pads. Cell nuclear levels of radioactivity peaked at 1 h in both hypothalamus and parametrial adipose tissue, but the peak cell nuclear concentration in the fat pad was more than twice that in hypothalamus. At 1 h, 89% of the adipose tissue nuclear radioactivity migrated with 17 beta-estradiol on thin-layer plates. Radioactivity was retained in cell nuclei for more than 6 h in both tissues. This cell nuclear binding was estrogen specific. Pretreatment with radioinert estrogens (17 beta-estradiol or R 2858) abolished cell nuclear 17 beta-[3H]estradiol uptake, but other steroids (progesterone, corticosterone, and 5 alpha-dihydrotestosterone) were without effect. Cell nuclear binding was found in all fat pads studied in both males and females. Levels were highest in parametrial (females) and epididymal (males) fat pads, the depots with the highest concentration of cytoplasmic estrogen receptor. There were no sex differences in cell nuclear binding. Taken together these findings provide strong support for the contention that 17 beta-estradiol could affect lipid metabolism and body fat content in part by direct action on adipose tissues.

Prepubertal ontogeny of responsiveness to estradiol in female rat central nervous system.

The physiological response to systemic estrogens changes dramatically during the period from birth to puberty. With the onset of puberty, the rat reaches a critical developmental plateau with regard to endocrinological responsiveness to estradiol. Since the appearance of the pubertal response pattern appears to be less a consequence of some intrinsic "trigger' than the natural continuation of a developmental sequence that begins prenatally, its ontogeny should be examined in a broad context that will take account of the impact of each of the dynamic components influencing the interactions between estradiol and the central nervous system on the functional development of the organism as a whole. The prepubertal ontogeny of endocrinological responsiveness to estradiol in the central nervous system of the female rat is examined in the context of several of the important factors that are known to influence the functional development of the hypothalamo-pituitary-gonadal circuit:the rapidly changing hormonal environment of the morphologically and physiologically immature juvenile rat, the shifting predominance of alphafetoprotein and "adult" estradiol-binding protein, sexual differentiation of the neural substrate, and the development of mature pituitary-gonadal feedback mechanisms. The availability of ever more sensitive techniques for the measurement of the actions of estradiol in the central nervous system of the immature organism has necessitated a re-evaluation of existing data. This, in turn, suggests that new approaches should be applied to the examination of problems related to the development of reproductive maturity of the central nervous system.