Estradiol receptor levels in rat hypothalamic and limbic nuclei

Rainbow, T. C.; Parsons, Bruce; Nj, MacLusky; McEwen, BS

doi:10.1523/jneurosci.02-10-01439.1982

Cited by 140 publications

(30 citation statements)

References 26 publications

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“…Comparison of our present data with that presented for estrogen receptors in our companion paper (Rainbow et al, 1982b) suggests, but does not prove, that some brain regions which contain estrogen receptors lack the capacity to form progestin receptors in response to Ez. For example, both the medial and cortical amygdala contain estrogen receptors, but only the medial amydala shows a significant CPR induction following EZ treatment.…”

Section: Methodscontrasting

confidence: 89%

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Progestin receptor levels in rat hypothalamic and limbic nuclei

Parsons¹,

Rainbow²,

Nj³

et al. 1982

J. Neurosci.

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257

108

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We have utilized a method to minimize cytosol progestin receptor loss during freezing in order to localize and quantify estrogen-inducible progestin receptors in individual nuclei of the female rat brain.Ovariectomized females received estradiol benzoate (20 pg for 3 days) or vehicle prior to sacrifice. All animals were perfused with cold distilled Hz0 containing the cryoprotective compound, dimethyl sulfoxide (DMSO; 10% (v/v)). Thirty-one nuclei or brain regions were removed from frozen sections (300 pm) according to the method of Palkovits (Palkovits, M. (1973) Brain Res. 59: 449-450) and were assayed in vitro using a synthetic radioligand, r3H]R5020.In ovariectomized animals perfused with DMSO, a basal level (1 to 8 fmol/mg of protein) of progestin receptors was observed in a variety of preoptic, hypothalamic, and limbic structures. Moreover, estrogen treatment induced high levels (24 to 49 fmol/mg of protein) of progestin receptors in regions of the preoptic area of hypothalamus which contain high levels of estrogen receptors. These regions included the medial, periventricular, and superchiasmatic nuclei of the preoptic area, the periventricular anterior hypothalamus, the ventromedial nucleus, and the arcuatemedian eminence. Moderate levels (2 to 8 fmol/mg of protein) of progestin receptors were induced by estrogen in other hypothalamic and limbic structures, including the anterior and lateral hypothalamus, the bed nucleus of the stria terminalis, the cingulate cortex, the medial amygdaloid nucleus, and the CA, subfield of the hippocampus. By contrast, some areas, such .as the caudateputamen and the supraoptic nucleus, were devoid of both estrogen-inducible and uninduced progestin receptors.These results support the hypothesis that progesterone action in the central nervous system is mediated by cytosol receptors in discrete brain regions and provide the first quantitative map of progestin binding in a vertebrate brain.Progesterone (P) and estradiol (E2) synergize to activate feminine reproductive behavior and to induce gonadotropin secretion in a number of vertebrate species, including the rat and guinea pig. Previous studies which have employed [3H]progesterone as a radioligand usually have failed to identify specific progestin-binding components which could mediate the central actions of P in the vertebrate brain (for references, see Feder and Marrone, 1978;McEwen, 1978).

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Section: Methodscontrasting

confidence: 89%

“…This concentration of C3H] R5020 was selected to bind specifically the high, but not low, affinity progestin binding site present in brain . Bound [3H]R5020 was measured by gel filtration on "miniature" Sephadex LH-20 (Pharmacia) columns as described in our companion paper (Rainbow et al, 1982b).…”

Section: Methodsmentioning

confidence: 99%

Progestin receptor levels in rat hypothalamic and limbic nuclei

Parsons¹,

Rainbow²,

Nj³

et al. 1982

J. Neurosci.

Self Cite

257

108

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“…What is the mechanism by which a previously unresponsive neuronal type becomes responsive? Although estrogens can act to alter gene transcription (McEwen et al, 1978), it is unlikely that this is the case in the present study because in the hippocampus, both ␣-and ␤-estrogen receptors have been identified on interneurons and glial cells and not on dentate granule cells (Rainbow et al, 1982;L oy et al, 1988;Pelletier et al, 1988;Weiland et al, 1996;Kuiper et al, 1997;Li et al, 1997). Estradiol might act directly on membranes, altering their properties to induce glutamate release, thus increasing intraneuronal calcium, stimulating NMDA receptors, leading to the addition of dendritic spines (Parpura et al, 1994;Woolley and McEwen, 1994;K lintsova et al, 1995).…”

Section: Discussionmentioning

confidence: 63%

Granule Cells in Aging Rats Are Sexually Dimorphic in Their Response to Estradiol

1999

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Normal aging comprises cognitive decline, including deterioration of memory. It has been suggested that this decline in memory is sexually dimorphic because of the cessation in gonadal steroid secretion that occurs during reproductive aging in female, but not male, mammals. We wondered whether neurons in brain regions associated with learning and memory underwent morphological changes that were dimorphic as well and whether cessation of the secretion of gonadal steroids influenced these morphological changes. To explore these questions, we deprived and restored estrogens to young and old gonadectomized females and males and studied the morphology of dentate granule cells by intracellular dye filling in a lightly fixed slice preparation. We found the following: (1) Aged female dentate granule cells deprived of gonadal steroids longterm have a paucity of dendritic spines compared with young females deprived short-term; however, aged male dentate granule cells deprived of gonadal steroids long-term have no decrease in dendritic spines compared with young males deprived short-term. (2) Aged female dentate granule cells with long-term estrogen replacement at either high or low levels still had a decline in spine density. (3) Aged female dentate granule cells with short-term estradiol replacement had spine density increased to levels normally observed in young adults, whereas aged males with short-term estradiol replacement had decreased spine density. These data suggest that the response of rat dentate granule cells to aging and estradiol is sexually dimorphic and that, in females, the responsiveness of granule cells depends on the temporal pattern of estradiol replacement.

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“…However, several animal studies in the literature discuss regionally specific trophic effects induced by the introduction of gonadal steroid hormones (for a review, see Jones, 1988). Some of the highest concentrations of steroid hormone receptors in rats are found in the hippocampus, amygdala, hypothalamus, and septal nuclei (Rainbow, Parsons, McLusky, & McEwen, 1982;Stumph & Sar, 1978), all of which are within our anterior diencephalic and MTL regions. Perhaps the increase in circulating gonadal steroid hormones that occurs at puberty has organizational effects on the morphology of the human brain.…”

Section: Asymmetry Analysesmentioning

confidence: 99%

Further MRI evidence of late brain maturation: Limbic volume increases and changing asymmetries during childhood and adolescence

Jernigan

1998

Developmental Neuropsychology

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Estradiol receptor levels in rat hypothalamic and limbic nuclei

Cited by 140 publications

References 26 publications

Progestin receptor levels in rat hypothalamic and limbic nuclei

Progestin receptor levels in rat hypothalamic and limbic nuclei

Granule Cells in Aging Rats Are Sexually Dimorphic in Their Response to Estradiol

Further MRI evidence of late brain maturation: Limbic volume increases and changing asymmetries during childhood and adolescence

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