Estrogen receptor‐β, but not estrogen receptor‐α, is expressed in prolactin neurons of the female rat paraventricular and supraoptic nuclei: Comparison with other neuropeptides

Suzuki, Shotaro; Handa, Robert J.

doi:10.1002/cne.20457

Cited by 90 publications

(112 citation statements)

References 99 publications

(150 reference statements)

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“…This suggests that by binding to ERbeta, estradiol could directly alter the function of PVN neuropeptide neurons. In contrast, ERalpha is found at low levels and only in the periventricular PVN and never in CRH, AVP or OXY neurons (Simerly et al, 1991;Estacio et al, 1996;Suzuki and Handa, 2005) thereby ruling out a direct estradiol action mediated through ERalpha, on PVN responses to stress.…”

Section: Neural Androgen Receptor and Estrogen Receptor Distribution mentioning

confidence: 95%

“…A large percent of ERbeta-ir cells in PVN are AVP positive, but ERbeta is also found in many oxytocin, prolactin (Somponun andSladek, 2004a, Hrabovsky et al, 1998;Alves et al, 1998;Suzuki and Handa, 2005) and some CRH containing neurons of the PVN (LaFlamme et al, 1998;Miller et al, 2004, Suzuki and. This suggests that by binding to ERbeta, estradiol could directly alter the function of PVN neuropeptide neurons.…”

Section: Neural Androgen Receptor and Estrogen Receptor Distribution mentioning

confidence: 99%

“…Vasopressin containing cells in the PVN and SON contain ERbeta (Suzuki and Handa, 2005;LaFlamme et al, 1998) suggesting a direct regulation of AVP gene expression by ERbeta. To test whether 3β-Diol can have direct effects on the AVP promoter, reporter gene assays were employed.…”

Section: -β-Diol Regulation Of Gene Promotersmentioning

confidence: 99%

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An alternate pathway for androgen regulation of brain function: Activation of estrogen receptor beta by the metabolite of dihydrotestosterone, 5α-androstane-3β,17β-diol

Handa

Pak

Kudwa

et al. 2008

Hormones and Behavior

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182

122

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The complexity of gonadal steroid hormone actions is reflected in their broad and diverse effects on a host of integrated systems including reproductive physiology, sexual behavior, stress responses, immune function, cognition, and neural protection. Understanding the specific contributions of androgens and estrogens in neurons that mediate these important biological processes is central to the study of neuroendocrinology. Of particular interest in recent years has been the biological role of androgen metabolites. The goal of this review is to highlight recent data delineating the specific brain targets for the dihydrotestosterone metabolite, 5α-androstane, 3β, 17β-diol (3β-Diol). Studies using both in vitro and in vivo approaches provide compelling evidence that 3β-Diol is an important modulator of the stress response mediated by the hypothalmo-pituitary-adrenal axis. Further, the actions of 3β-Diol are mediated by estrogen receptors, and not androgen receptors, often through a canonical estrogen response element in the promoter of a given target gene. These novel findings compel us to re-evaluate the interpretation of past studies and the design of future experiments aimed at elucidating the specific effects of androgen receptor signaling pathways.

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Section: Neural Androgen Receptor and Estrogen Receptor Distribution mentioning

confidence: 95%

Section: Neural Androgen Receptor and Estrogen Receptor Distribution mentioning

confidence: 99%

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An alternate pathway for androgen regulation of brain function: Activation of estrogen receptor beta by the metabolite of dihydrotestosterone, 5α-androstane-3β,17β-diol

Handa

Pak

Kudwa

et al. 2008

Hormones and Behavior

Self Cite

182

122

View full text Add to dashboard Cite

show abstract

“…Double IHC for Fos and GnRH protein was performed as described previously (Suzuki and Handa, 2005). Briefly, tissue was washed three times in PBS with 0.1% Triton X-100 (PBST) and blocked for 15 min in 0.3% H 2 O 2 .…”

Section: Double-label Ihc For Fos and Gnrhmentioning

confidence: 99%

The Role of Kisspeptin–GPR54 Signaling in the Tonic Regulation and Surge Release of Gonadotropin-Releasing Hormone/Luteinizing Hormone

Dungan¹,

Gottsch²,

Zeng³

et al. 2007

J. Neurosci.

194

144

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The Kiss1 gene codes for kisspeptin, which binds to GPR54, a G-protein-coupled receptor. Kisspeptin and GPR54 are expressed in discrete regions of the forebrain, and they have been implicated in the neuroendocrine regulation of reproduction. Kiss1-expressing neurons are thought to regulate the secretion of gonadotropin-releasing hormone (GnRH) and thus coordinate the estrous cycle in rodents; however, the precise role of kisspeptin-GPR54 signaling in the regulation of gonadotropin secretion is unknown. In this study, we used female mice with deletions in the GPR54 gene [GPR54 knock-outs (KOs)] to test the hypothesis that kisspeptin-GPR54 signaling provides the drive necessary for tonic GnRH/luteinizing hormone (LH) release. We predicted that tonic GnRH/LH secretion would be disrupted in GPR54 KOs and that such animals would be incapable of showing a compensatory rise in LH secretion after ovariectomy. As predicted, we found that GPR54 KO mice do not exhibit a postovariectomy rise in LH, suggesting that tonic GnRH secretion is disrupted in the absence of kisspeptin-GPR54 signaling. We also postulated that kisspeptin-GPR54 signaling is critical for the generation of the estradiol (E)-induced GnRH/LH surge and thus E should be incapable of inducing an LH surge in the absence of GPR54. However, we found that E induced Fos expression in GnRH neurons and produced a GnRH-dependent LH surge in GPR54 KOs. Thus, in mice, kisspeptin-GPR54 signaling is required for the tonic stimulation of GnRH/LH secretion but is not required for generating the E-induced GnRH/LH surge.

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“…This is further supported by our anatomical evidence showing the coexistence of Ucn mRNA and ER␤ in the same PVN cells. We were not able to obtain consistent results regarding the presence of ER␣ in the PVN; however, the presence of ER␣ in the PVN has been documented in rats (Suzuki and Handa, 2005) and humans (Bao et al 2005). Additional studies would be appropriate to address whether Ucn and ER␣ coexist in the same PVN neurons.…”

Section: Discussionmentioning

confidence: 70%

Estrogen Receptors α and β Differentially Regulate the Transcriptional Activity of the Urocortin Gene

Haeger¹,

Andrés²,

Forray³

et al. 2006

J. Neurosci.

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Urocortin (Ucn), a highly conserved metazoan gene, is related to stress and feeding, behaviors with significant gender differences. We investigated whether estrogens regulate the expression of the Ucn gene using transient transfection in PC12 cells with the human Ucn (hUcn) promoter coupled to luciferase and either ␣ or ␤ estrogen receptors (ER␣ or ER␤, respectively). The results demonstrate that estradiol (E 2 ) increases the activity of the hUcn promoter via ER␣, and decreases hUcn promoter activity through ER␤. Deletions of the hUcn promoter show that the increase in promoter activity mediated by E 2 -ER␣ depends on a promoter region containing a half-estrogen response element and an Sp1 site, and the decrease mediated by E 2 -ER␤ depends on a proximal promoter region containing a cAMP response element. Ucn and ERs coexist in neurons of rat hypothalamic nuclei, giving anatomical support for a direct effect of estrogen receptors on the Ucn gene. By in situ hybridization, we observed that cycling female rats have a higher number of cells expressing Ucn mRNA than males in the paraventricular nucleus of the hypothalamus (PVN) and the septum. Both of these brain nuclei are related to stress behaviors and express moderate levels of Ucn. Furthermore, Ucn mRNA was significantly decreased in the PVN and increased in the septum 30 d after ovariectomy. Acute E 2 administration to ovariectomized rats significantly increased Ucn mRNA expression in the PVN and septum. In conclusion, our in vitro and in vivo evidence suggests that estrogens exert a direct and differential transcriptional regulation of the Ucn gene.

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Estrogen receptor‐β, but not estrogen receptor‐α, is expressed in prolactin neurons of the female rat paraventricular and supraoptic nuclei: Comparison with other neuropeptides

Cited by 90 publications

References 99 publications

An alternate pathway for androgen regulation of brain function: Activation of estrogen receptor beta by the metabolite of dihydrotestosterone, 5α-androstane-3β,17β-diol

An alternate pathway for androgen regulation of brain function: Activation of estrogen receptor beta by the metabolite of dihydrotestosterone, 5α-androstane-3β,17β-diol

The Role of Kisspeptin–GPR54 Signaling in the Tonic Regulation and Surge Release of Gonadotropin-Releasing Hormone/Luteinizing Hormone

Estrogen Receptors α and β Differentially Regulate the Transcriptional Activity of the Urocortin Gene

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