Localization of hypothalamic sites for the estrogen-priming of sexual receptivity in female hamsters.

Floody, Owen R.; Blinn, Nancy E.; Lisk, Robert D.; Vomachka, Archie J.

doi:10.1037/0735-7044.101.3.309

Cited by 22 publications

(9 citation statements)

References 9 publications

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“…These findings support the hypothesis that the reduced behavioral responsiveness to exogenous steroids in fuel-deprived, ovariectomized hamsters is at least in part due to a decrease in estradiol binding in the VMH/VLH. The VMH is probably a pivotal locus for the facilitation of lordosis by estradiol and progesterone (19,37,38). In female hamsters, bilateral lesions in the VMH eliminate steroid-induced lordosis (21), whereas implants of estradiol restricted to the VMH are sufficient to facilitate female sexual behavior (19,37,38).…”

Section: Discussionmentioning

confidence: 99%

“…The VMH is probably a pivotal locus for the facilitation of lordosis by estradiol and progesterone (19,37,38). In female hamsters, bilateral lesions in the VMH eliminate steroid-induced lordosis (21), whereas implants of estradiol restricted to the VMH are sufficient to facilitate female sexual behavior (19,37,38). Moreover, an antiestrogen applied directly to the VMH can block the expression of lordosis in rats (39), indicating that estradiol specifically in the VMH is necessary for lordosis.…”

Section: Discussionmentioning

confidence: 99%

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Manipulations of metabolic fuel availability alter estrous behavior and neural estrogen receptor immunoreactivity in Syrian hamsters.

Wade

Blaustein

1994

Endocrinology

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Decreases in metabolic fuel utilization caused by food deprivation, diabetes, or treatment with metabolic inhibitors have been shown to suppress steroid-induced estrous behavior in ovariectomized Syrian hamsters. These same manipulations also caused a decrease in the number of detectable estrogen-receptor immunoreactive (ERIR) cells in the ventromedial hypothalamus (VMH) and the adjacent area lateral to it (VLH) in ovariectomized hamsters. Forty-eight hours of food deprivation or treatment with pharmacological blockers of glycolysis (2-deoxy-D-glucose) and fatty acid oxidation (methyl palmoxirate) decreased the number of detectable ERIR cells in the VMH/VLH. However, neither inhibitor given alone was sufficient to affect the number of detectable ERIR cells in the VMH/VLH, even when given in much higher doses. Therefore, the number of ERIR cells in the VMH/VLH, like steroid-induced estrous behavior, responds only to a combination of glucoprivation and lipoprivation and not to either alone. The effects of metabolic fuel restriction are not due to a general suppression of neural ERIR, because food deprivation or treatment with 2-deoxy-D-glucose and methyl palmoxirate actually increased the number of detectable ERIR cells in the medial preoptic area (mPOA) and had no effect in the nucleus of the solitary tract. Lesions destroying the area postrema (AP) prevented the decrease in ERIR cells in the VMH/VLH and the inhibition of estrous behavior caused by fuel restriction. However, AP lesions did not alter the effects of metabolic inhibitors on ERIR in the mPOA. On the other hand, subdiaphragmatic vagotomy abolished the effects of metabolic inhibitors on mPOA ERIR, but did not affect either lordosis or VMH/VLH ERIR. These results suggest that the suppression of estrous behavior induced by metabolic fuel restriction is at least in part due to a decrease in the number of ERIR neurons in the VMH/VLH. In addition, the estrogen-sensitive neurons in the VMH/VLH and mPOA receive metabolic cues via different neural pathways. The AP, but not vagus nerves, is required for ERIR neurons in the VMH/VLH to detect fuel availability; the vagus nerves, but not the AP, are necessary for estrogen-binding neurons in the mPOA to detect visceral information.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Manipulations of metabolic fuel availability alter estrous behavior and neural estrogen receptor immunoreactivity in Syrian hamsters.

Wade

Blaustein

1994

Endocrinology

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“…This work has also shown that manipulations of metabolic fuel availability increase ERIR in the medial preoptic area (MPO) and have no effect on ERIR in the nucleus of the solitary tract in OVX hamsters. These findings suggest that suppression of hamster estrous behavior by food deprivation is due, at least in part, to a decrease in ERIR in the VMH/VLH, a critical site involved in regulation of estrous behavior by estradiol and progesterone (10,12,18,22,26).…”

mentioning

confidence: 88%

Effects of food deprivation on induction of neural progestin receptors by estradiol in Syrian hamsters

Wade

Blaustein

1996

American Journal of Physiology-Regulatory, Integrative and Comp

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-Food deprivation, as well as treatment with metabolic inhibitors, suppresses steroid hormone-induced estrous behavior in ovariectomized (OVX) Syrian hamsters. Previous work indicates that 48 h of food deprivation decreases the number of detectable estrogen-receptor immunoreactive (ERIR) cells in the ventromedial hypothalamus (VMH) and the area just lateral to it (VLH), increases the number of ERIR cells in the medial preoptic area (MPO), and has no effect on the number of ERIR cells in the nucleus of the solitary tract in OVX hamsters. The present study examined the effects of food deprivation on neural progestin receptor binding using an in vitro binding assay and on progestin receptor immunoreactivity (PRIR) in estradiol-primed, OVX hamsters. Parallel behavior tests for sexual behavior were also performed in both experiments. OVX hamsters received 2.5 µg estradiol benzoate (EB) and were fed ad libitum or food deprived at the same time. Forty-eight h later, animals were killed in preparation for the immunocytochemistry or progestin receptor assay. Binding assays indicated that 48 h food deprivation decreased progestin receptor levels in the preoptic area and had no effect in the mediobasal hypothalamus, an area which includes the VMH and the arcuate nucleus (ARH). Immunocytochemical analysis confirmed these findings. Food deprivation caused a decrease in sexual receptivity and in the number of detectable PRIR cells in the MPO and medial amygdala but had no effect on the number of detectable PRIR cells in the VMH/VLH, the ARH, or the anteroventral periventricular nucleus. These results suggest that food deprivation modulates progestin receptor binding and PRIR in a site-specific manner. In addition, the effects of food deprivation on neural ERIR and PRIR are significantly different. nutritional infertility, progestin receptor, estrogen receptor, estrous behavior, hamsters, ventromedial hypothalamus, preoptic area MANY ENVIRONMENTAL FACTORS, including food availability, photoperiod, temperature, and social cues, can influence the reproductive performance of mammals. Almost every component of reproduction including puberty, ovulation, reproductive behavior, and lactation demand energy. Therefore, it is not surprising that food availability is one of the most important factors regulating mammalian reproduction (8). In female mammals, undernutrition delays puberty, interrupts menstrual and estrous cycles (8,30) and prevents the occurrence of estrous behavior in a variety of species, including hamsters (11,17,20). The neural mechanisms underlying nutritional infertility have attracted a great deal of interest. Food restriction alters the secretion of pituitary gonadotropins and gonadal steroids. This response is thought to be primarily due to the suppression of GnRH release (8,16,23,30). The activity of GnRH neurons in forebrain of underfed hamsters appears to decrease, which is reflected by the suppression of Fos-like immunoreactivity (1). In addition to the influence of metabolic manipulations on reproductive phys...

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“…This is the case when E2 is given alone or in conjunction with progesterone (P 4). Interestingly, plasma levels o f total androgens have been measured in sex ually receptive females and are typically 8-10 times higher than E ; levels [28],In the majority o f female mammals investigated in the labo ratory, the expression o f sexual behavior is dependent on the presence o f appropriate external and internal conditions, typi cally including sufficient circulating and brain concentrations of ovarian steroids [13,14, 31, 38], In most species, ovariectomy eliminates sexual behavior, while hormone replacement studies have shown that E?, in some species acting synergistically with P4, reinstates sexual behavior to normal levels [2,13, 39], In the few species where sexual behavior persists after ovariectomy, steroids secreted by the adrenal gland may play an important role in the activation o f sexual behavior. In these species, andro gens either in addition to, or in place of, estrogens may regulate the expression o f female sexual behavior [1,12,21, 33].…”

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confidence: 99%

Role of Androgens in the Regulation of Sexual Behavior in the Female Musk Shrew

1990

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These experiments were conducted to determine whether androgens are involved in the regulation of female sexual behavior in the musk shrew (Suncus murinus). In the musk shrew, sexual behavior can be reinstated after ovariectomy by the administration of supraphysiological doses of either estradiol (E₂) or testosterone. However, physiological doses of E₂ are not effective in this regard. To examine the role of androgens, ovariectomized (OVX) females received testosterone-filled hormone implants. These implants reinstated sexual behavior in a dose-dependent manner. To determine whether the aromatization of androgen is essental for restoration of sexual behavior, the nonaromatizable androgen, dihydrotestosterone (DHT), was administered to OVX females either alone or with an implant containing E₂; sexual behavior was not restored. In the third experiment, gonadally intact females, treated with the aromatization inhibitor l,4,6-androstatriene-3,17-dione (ATD) exhibited no sexual behavior and had significantly lower levels of aromatase activity in the medial basal hypothalamus/preoptic area than control females. In the last experiment, OVX females implanted with testosterone and given concurrent ATD treatment demonstrated significantly less sexual behavior as compared with controls. These results suggest that either estrogens produced via androgen aromatization in the brain and/or an intermediate product in the aromatization process are involved in the regulation of sexual behavior in the female musk shrew.

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Localization of hypothalamic sites for the estrogen-priming of sexual receptivity in female hamsters.

Cited by 22 publications

References 9 publications

Manipulations of metabolic fuel availability alter estrous behavior and neural estrogen receptor immunoreactivity in Syrian hamsters.

Manipulations of metabolic fuel availability alter estrous behavior and neural estrogen receptor immunoreactivity in Syrian hamsters.

Effects of food deprivation on induction of neural progestin receptors by estradiol in Syrian hamsters

Role of Androgens in the Regulation of Sexual Behavior in the Female Musk Shrew

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