In Vivo Progesterone Treatment Enhances [3H\Estradiol Retention by Neural Tissue of the Female Rat
TL;DR: The demonstration that progesterone pretreatment can significantly increase [3H]estradiol retention by neural tissue suggests a possible mechanism by which progester one can regulate the timing of ovulation and sex behavior.
Abstract: [3H]Estradiol retention was examined for neural tissues of ovariectomized rats as a function of various progesterone pretreatments. Short-term progesterone pretreatment (6 or 24 h) with a 50 mg pellet of progesteron sc resulted in increased in vivo retention of [3H]estradiol when measured at 6 or 24 h following withdrawal of the progesterone source. This increase was greatest in arcuate-median eminence tissue. A less pronounced increase was seen in the preoptic-anterior hypothalamus and cerebral cortex, and no increase was seen in the amygdala or mammilary bodies. Following long term progesterone pretreatment increased [3H]estradiol retention was observed in vivo at 48, 72, 96 or 120 h in the continued presence of the progesterone source for arcuate-median eminence, preoptic-anterior hypothalamus, amygdala and cerebral cortex. Also, when progesterone pretreatment was 24 h, [3H]estradiol retention was still increased at 36, 48, 60 and 72 h following removal of the progesterone source for arcuate-median eminence, preoptic-anterior hypothalamus, amygdala and cerebral cortex. Our demonstration that progesterone pretreatment can significantly increase [3H]estradiol retention by neural tissue suggests a possible mechanism by which progesterone can regulate the timing of ovulation and sex behavior. Furthermore, our observations are in keeping with the finding that progesterone has little or no effect at the organismal or tissue level unless estrogen is present.
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TL;DR: In the ovariectomized rat, induction of PR followed the same pattern as induction of lordosis, and the increase in PR after EB priming was lower and in accord with the much higher EB doses required for a lordosis response.
Abstract: Modifications in the concentration of progestinbinding sites (PR) in rat hypothalamus and pituitary, measured with [3H]R5020 (promegestone, 17,21-dimethyl-19-nor-4,9-pregnadiene-3,20-dione) have been related to the facilitative and inhibitory actions of progesterone (P) oh female sexual behavior. In the ovariectomized rat, induction of PR followed the same pattern as induction of lordosis. Exposure of the brain to estrogens for less than 12 h is ineffective in bringing about lordosis and did not increase PR. The optimal interval between estrogen and P administration for lordosis is 24–48 h; the maximum increase in PR took place 24–48 h after estrogen priming. This induction was estrogen dose dependent; the dose of estradiol benzoate (EB) required for lordosis (2-5 μg/rat) produced a 2-fold increase in PR after 40 h. In males, the increase in PR after EB priming was lower and in accord with the much higher EB doses required for a lordosis response. When a large dose of P was injected simultaneously with EB...
159 citations
01 Jan 1989
TL;DR: This chapter presents a neuroethological analysis of maternal behavior, with emphasis on nursing behavior and its immediate antecedents, and indicates that the control of maternal aggression is similar to that of pup retrieval and licking with respect to perioral somatosensory regulation but apparently different withrespect to the importance of additional olfactory and ventral somatoensory determinants.
Abstract: Publisher Summary This chapter presents a neuroethological analysis of maternal behavior, with emphasis on nursing behavior and its immediate antecedents. A comprehensive neuroethological analysis of mammalian maternal behavior, grounded in an understanding of the sensory, neural, and motor mechanisms, has been impeded in large part by the complexity of maternal behavior. The sight, sound, and smell of pups are all neural stimuli to which rat mothers are responsive. This facilitates their localization of pups displaced from the nest. The hormones contribute to the onset of maternal behavior. They are responsible for maternal aggression, nest building, and fearfulness. In addition to this priming role of hormones, the hormones also influence the maternal behavior indirectly during lactation. The delineation of neural circuits underlying the expression of each component of maternal behavior requires separate analyses. The control of maternal aggression is similar to that of pup retrieval and licking with respect to perioral somatosensory regulation but apparently different with respect to the importance of additional olfactory and ventral somatosensory determinants.
129 citations
TL;DR: Modulation by progesterone of the estrogen-induced LH surge does not seem to result from effects on neural and hypophysial estrogen receptors, and suppression of uterine estrogen receptors by progestersone may account in part for antagonism by this steroid of estrogen-stimulated uterine growth.
Abstract: The possibility that inhibition and facilitation of estrogen-induced LH surges by progesterone could be associated with effects of this steroid on the concentration, subcellular distribution, or molecular properties of estrogen receptors in the hypothalamus-preoptic area (HPOA) and pituitary was investigated. Immature rats (28 days old) that received Silastic capsules containing estradiol-17 beta in oil (150 micrograms/ml) at 0900 h had LH surges between 1700 and 2000 h on day 29. This treatment led to depletion of cytoplasmic estrogen receptors (to 25-35% of control levels) and their accumulation in the nucleus. Insertion of crystalline progesterone implants concomitantly with estradiol implants or 24 h later resulted in blockade or enhancement of the LH surge, respectively. Progesterone administered in either mode did not significantly after the levels of estrogen receptors in the HPOA and pituitary; however, progesterone did suppress the quantity of both cytoplasmic and nuclear estrogen receptors in the uterus when administered in conjunction with estradiol for 24 h oe for 8 h after 24-h estrogen priming. The binding affinity and sedimentation properties in sucrose gradients of cytoplasmic estrogen receptors were unchanged by progesterone treatment. The specificity of the effects of progesterone on LH secretion was examined. Testosterone, dexamethasone, and the synthetic progestin R5020 (17,21-dimethyl-19-nor-4,9-pregnadien-3,20-dione) also inhibited LH surges when injected 8 h after placement of estradiol implants in 28-day-old rats. Only progesterone and R5020 brought about premature and sustained LH release when given to estradiol-primed rats at 0900 h on day 29. None of these compounds interfered directly with the binding of [3H]estradiol to cytoplasmic or nuclear receptors. In conclusion, modulation by progesterone of the estrogen-induced LH surge does not seem to result from effects on neural and hypophysial estrogen receptors. In contrast, suppression of uterine estrogen receptors by progesterone may account in part for antagonism by this steroid of estrogen-stimulated uterine growth.
56 citations
TL;DR: Investigation of the influence of progesterone on the concentration of estrogen receptors in the hypothalamus-preoptic area, anterior pituitary gland, and uterus of chronically estradiol-treated ovariectomized rats demonstrates that, under some conditions, progester one decreases HP and AP estrogen receptor concentrations.
45 citations
01 Jan 1985
TL;DR: It is well established that progesterone plays a role in the brain and hypophysis as a facilitator and inhibitor of sexual behavior and gonadotropin release in the female rat.
Abstract: It is well established that progesterone plays a role in the brain and hypophysis as a facilitator and inhibitor of sexual behavior and gonadotropin release in the female rat (Everett 1961; Caligaris et al. 1971; Brown-Grant and Naftolin 1972; Dorner 1972; Meyerson 1972; Barraclough 1973; Goldman and Zarrow 1973; Mann and Barraclough 1973; Freeman et al. 1976; Feder and Marrone 1977; Goodman 1978; Attardi 1981), guinea pig (Morin and Feder 1974), and primates (Odell and Swerdloff 1968; Spies and Niswender 1972; Yamaji et al. 1972; Karsch et al. 1973; Dierschke et al. 1973; Knobil 1974; Clifton et al. 1975).
44 citations