Androgen Receptors and Estrogen Receptors Are Colocalized in Male Rat Hypothalamic and Limbic Neurons that Express Fos Immunoreactivity Induced by Mating

Greco, Béatrice; Edwards, David A.; Michael, Richard P.; Clancy, Andrew N.

doi:10.1159/000054294

Cited by 103 publications

(57 citation statements)

References 49 publications

(82 reference statements)

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“…Immunofluorescent visualization of neural proteins may in some cases be less sensitive than some other visualization techniques and may result in an underestimation of the number of neurons expressing the protein under investigation [41]. Therefore, as in all experiments of this type, our results may underestimate the number of Fos-ir, ERα-ir, and double-labeled neurons in the brains of lactating rats after our experimental manipulations rather than provide an absolute number of neurons that contain these proteins.…”

Section: Discussionmentioning

confidence: 99%

Maternal Behavior Stimulates <i>c-fos</i> Activity within Estrogen Receptor Alpha-Containing Neurons in Lactating Rats

et al. 2000

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Estradiol and other hormones are thought to be critical for the onset, but not maintenance, of maternal behavior in rats. Maternal behavior is instead maintained postpartum by tactile stimulation that dams receive during interactions with pups, and many neural sites implicated in the control of maternal behavior show elevated c-fos activity in response to this stimulation. Many of these sites also contain neurons that express the alpha subtype of the estrogen receptor (ERα). Because of possible interactions between tactile stimulation from pups, c-fos, and ERα in the lactating rat brain, we determined if populations of cells that show increased c-fos activity after maternal behavior in lactating rats also contain ERα. Dams were separated from their pups for 48 h beginning on day 5 postpartum. On day 7 postpartum, experimental dams were reunited with pups and mother-litter interactions were observed for 60 min. Control dams received no pup stimulation. Subjects were sacrificed 60 min later and brain sections were double immunolabeled for the Fos and ERα proteins. As expected, the number of ERα-immunoreactive (ERα-ir) neurons did not differ between the two groups in the eight areas analyzed (lateral region of the lateral septum, posterodorsal medial amygdala, dorsal and ventral medial preoptic area, dorsal and ventral bed nucleus of the stria terminalis, lateral habenula, and ventrolateral caudal periaqueductal gray). Consistent with previous reports, maternal dams had 2- to 7-fold more Fos-immunoreactive (Fos-ir) neurons in these sites compared with nonstimulated controls. Maternal dams had significantly more Fos-ir neurons that also contained ERα-ir in all sites, with the greatest increases in the ventral medial preoptic area, lateral habenula, and ventral bed nucleus of the stria terminalis. Between ∼25 and 45% of the Fos-ir cells in the sites examined also expressed ERα. Thus, a substantial number of neurons that are genomically activated during maternal behavior contain ERα, raising the possibility that the postpartum display of maternal behavior can be influenced by ERα activity.

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Section: Discussionmentioning

confidence: 99%

Maternal Behavior Stimulates <i>c-fos</i> Activity within Estrogen Receptor Alpha-Containing Neurons in Lactating Rats

et al. 2000

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“…The 1D5 monoclonal antibody is a very well characterized reagent, shown to bind to estrogen receptor ␣ in human endometrial and myometrial cells and normal and hyperplastic mammary epithelial cells, as well as some breast carcinoma epithelia. Similarly, this reagent has been used to identif y estrogen receptor ␣-containing cells in neurons, uteri, and growth plates of rats (Greco et al, 1998;Kennedy et al, 1999). After rinsing, the slides were sequentially exposed to biotinylated anti-mouse immunoglobulins, streptavidin conjugated to horseradish peroxidase, and 3,3Ј-diaminobenzidine chromogen in imidazole-HC l, containing hydrogen peroxide.…”

Section: Estrogen Receptor ␣ Immunocytochemistrymentioning

confidence: 99%

Sex Steroid Regulation of the Inflammatory Response: Sympathoadrenal Dependence in the Female Rat

et al. 1999

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To investigate the role of sex steroids in sex differences in the response of rats to the potent inflammatory mediator bradykinin (BK), we evaluated the effect of sex steroid manipulation on the magnitude of BK-induced synovial plasma extravasation (PE). The magnitude of BK-induced PE is markedly less in females. Ovariectomy of female rats increased BK-induced PE, and administration of 17␤-estradiol to ovariectomized female rats reconstituted the female phenotype. Castration in male rats decreased BK-induced PE, and administration of testosterone or its nonmetabolizable analog dihydrotestosterone reconstituted the male phenotype. The results of these experiments strongly support the role of both male and female sex steroids in sex differences in the inflammatory response.Because the stress axes are sexually dimorphic and are important in the regulation of the inflammatory response, we evaluated the contribution of the hypothalamic-pituitaryadrenal and the sympathoadrenal axes to sex differences in BK-induced PE. Neither hypophysectomy nor inhibition of corticosteroid synthesis affected BK-induced PE in female or male rats. Adrenal denervation in females produced the same magnitude increase in BK-induced PE as adrenalectomy or ovariectomy, suggesting that the adrenal medullary factor(s) in females may account for the female sex steroid effect on BK-induced PE. Furthermore, we have demonstrated that in female but not male rats, estrogen receptor ␣ immunoreactivity is present on medullary but not cortical cells in the adrenal gland. These data suggest that regulation of the inflammatory response by female sex steroids is strongly dependent on the sympathoadrenal axis, possibly by its action on estrogen receptors on adrenal medullary cells.

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“…In female rats, receptivity (evidenced by lordosis) is mediated by an interconnected neuronal network composed of steroid-responsive (estrogen-responsive) cells [4, 5]. Presumably, a similar steroid-activated system or pathway governs the display of male copulatory behavior, an idea supported by the presence of estrogen receptors (ER) and/or androgen receptors colocalized with mating-induced Fos-ir in neurons of the medial preoptic area (MPO), the medial amygdala (MEA), the central tegmental field, the bed nucleus of the stria terminalis, and other areas known to mediate mating behavior [6]. …”

Section: Introductionmentioning

confidence: 99%

Effects of Estrogen in the Male Rat Medial Amygdala: Infusion of an Aromatase Inhibitor Lowers Mating and Bovine Serum Albumin-Conjugated Estradiol Implants Do Not Promote Mating

Huddleston

Paisley

Clancy³

2006

Neuroendocrinology

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In male rats, copulatory behavior depends on estrogen-responsive neurons located in brain areas known to be crucial for mating. Blocking the aromatization of testosterone (T) to estradiol (E₂) either throughout the brain or within the medial preoptic area (MPO) reduces mating, whereas E₂ treatment of either the MPO or the medial amygdala (MEA) maintains sexual behavior. The effects of T aromatization in the MEA have received less attention; therefore, 2 studies were done to further elucidate the effects of E₂ in the MEA. In experiment 1, gonadally intact male rats that showed robust mating behavior were administered chronic fadrozole, a nonsteroidal aromatase inhibitor, to the MEA to stop the conversion of T to E₂ and then paired with receptive females. Infusion of fadrozole to the MEA significantly lowered mating behavior in experimental males compared to vehicle-infused control males. To further investigate the mechanism by which E₂ acts in the MEA, in experiment 2, E₂ conjugated to bovine serum albumin (BSA-E₂: a complex of E₂and a large protein that does not cross the plasma membrane, thereby restricting the action of E₂ to cell-surface signaling) was chronically administered bilaterally to the MEA of castrated, dihydrotestosterone-treated males. This treatment did not maintain mating behavior. These studies show that E₂ acts in the MEA to promote male sexual behavior and suggest an intercellular mechanism of E₂ action.

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Androgen Receptors and Estrogen Receptors Are Colocalized in Male Rat Hypothalamic and Limbic Neurons that Express Fos Immunoreactivity Induced by Mating

Cited by 103 publications

References 49 publications

Maternal Behavior Stimulates <i>c-fos</i> Activity within Estrogen Receptor Alpha-Containing Neurons in Lactating Rats

Maternal Behavior Stimulates <i>c-fos</i> Activity within Estrogen Receptor Alpha-Containing Neurons in Lactating Rats

Sex Steroid Regulation of the Inflammatory Response: Sympathoadrenal Dependence in the Female Rat

Effects of Estrogen in the Male Rat Medial Amygdala: Infusion of an Aromatase Inhibitor Lowers Mating and Bovine Serum Albumin-Conjugated Estradiol Implants Do Not Promote Mating

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