Persistent Estrus and Blockade of Progesterone-Induced Lh Release Follows Lesions Which Do Not Damage the Suprachiasmatic Nucleus12

Wiegand, Stanley J.; Terasawa, Ei; Bridson, William E.

doi:10.1210/endo-102-5-1645

Cited by 128 publications

(76 citation statements)

References 6 publications

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“…Lesions spreading over the AVPV induce persistent vaginal estrus, indicating that the AVPV is indispensable for regulation of the ovulatory surge of luteinizing hormone (16). The results of antisense oligonucleotide infusion, which prolonged vaginal estrus along with diminished ER␤ expression in the AVPV, implicate ER␤-positive neurons in this structure in the induction of ovulatory surge of luteinizing hormone.…”

Section: Discussionmentioning

confidence: 99%

Sexually dimorphic expression of estrogen receptor β in the anteroventral periventricular nucleus of the rat preoptic area: Implication in luteinizing hormone surge

Orikasa

Kondo

Hayashi

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

157

151

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Striking sex difference was detected in the expression of estrogen receptor (ER)␤E strogen plays critical roles in sexual differentiation of the developing brain and sex-specific regulation of reproductive neuroendocrinology in adults (1, 2). Cellular estrogen signaling is conveyed by nuclear estrogen receptors (ERs), which include the classical ER␣ as well as the recently cloned ER␤ (3). Both ERs are expressed in the preoptic area (POA), hypothalamus and limbic structures, which have been implicated in the regulation of reproduction (4-6). It is unclear, however, whether ER␤, like ER␣ (7), is expressed in a sex-specific manner (8, 9). Furthermore, the presence of both ERs in the same neurons could alter the specificity of the transcription by forming heterodimers (10) and might produce different responses to estrogen in different cells, depending on the ratios of ER␣ and ER␤ (11).Disruption of either ER␣ or ER␤ affects various aspects of reproduction. Female and male ER␣ knockout mice are infertile (12), and ER␤ knockout females have a reduced fecundity (13). Anovulation and polycystic or hemorrhagic ovary are present in the ER␣ knockouts (14). Reductions of ovulatory capacity and polycystic ovary occur in the ER␤ knockouts (13). The syndrome may be caused, at least partially, by the impairment in the central mechanism for the secretion of luteinizing hormone.The anteroventral periventricular nucleus (AVPV) is sexually dimorphic with over three times as many dopaminergic neurons in the female rat compared with males (15), and this supports the importance of this brain region in the control of estrous cyclicity, which is absent in males. Indeed, small lesions confined to the AVPV block the cyclic release of luteinizing hormone in female rat and results in anovulatory, persistent estrous state (16).Implantation of microcannulae containing antiestrogens into the AVPV suppressed spontaneous luteinizing hormone surges (17).In the present study, striking sex difference, detected in the ER␤ expression in the AVPV, was reversed by altering neonatal steroid environment. ER␤ mRNA and ER␣ immunoreactivity colocalized in many AVPV cells, some of which would be dopaminergic in nature. Infusion of ER␤ antisense oligonucleotides prolonged vaginal estrus and was accompanied by a 50% reduction of ER␤ immunoreactivity. Materials and MethodsSubjects. Female and male Sprague-Dawley rats (Saitama Experimental Animals, Saitama, Japan) were used on postnatal d 7, 14, 21, 35, or 60 (d 1 ϭ the day of birth) for brain morphometry. They were maintained in a controlled environment at 23°C with a 12-hr light͞12-h dark cycle (lights on at 11 a.m.). The weaning occurred on d 21. Free access to laboratory chow and water was allowed thereafter. A cohort of animals underwent endocrine manipulations as neonates or pups: males were orchidectomized under hypothermia on d 1; females received daily s.c. injections of 10 g 17␤-estradiol benzoate (Sigma) in oil on d 1 through d 10. All juvenile males and females were used without gonadectomy.ER␤ mRNA ...

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Section: Discussionmentioning

confidence: 99%

Sexually dimorphic expression of estrogen receptor β in the anteroventral periventricular nucleus of the rat preoptic area: Implication in luteinizing hormone surge

Orikasa

Kondo

Hayashi

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

157

151

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“…Thus, although both groups of neurons express Kiss1, it is likely that they serve different physiological functions. The AVPV is thought to contain neural circuits involved in generating GnRH/LH surges (Wiegand et al, 1978;Simerly, 1998). Kiss1 neurons in the AVPV express ER␣, and at the time of the preovulatory LH surge (in the rat), those same neurons express Fos and increase their synthesis of Kiss1 mRNA (Smith et al, 2006;Adachi et al, 2007).…”

Section: Discussionmentioning

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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“…Furthermore this structure has been found to play a critical role in regulating the cyclic release of gonadotropins in the female rats (Wiegand et al, 1978;Terasawa et al, 1980).…”

Section: Perinatal Androgen Exposure Decreases the Size O F The Sexuamentioning

confidence: 99%

“…Experimental and control animals were sacrificed at 90 days of age. (Wiegand et al, 1978;Terasawa et al 1980 …”

Section: Perinatal Androgen Exposure Decreases the Size O F The Sexuamentioning

confidence: 99%

Perinatal androgen exposure decreases the size of the sexually dimorphic medial preoptic nucleus in the rat.

Itō

Murakami²,

Yamanouchi³

et al. 1986

Proceedings of the Japan Academy. Ser. B: Physical and Biologic

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Persistent Estrus and Blockade of Progesterone-Induced Lh Release Follows Lesions Which Do Not Damage the Suprachiasmatic Nucleus12

Cited by 128 publications

References 6 publications

Sexually dimorphic expression of estrogen receptor β in the anteroventral periventricular nucleus of the rat preoptic area: Implication in luteinizing hormone surge

Sexually dimorphic expression of estrogen receptor β in the anteroventral periventricular nucleus of the rat preoptic area: Implication in luteinizing hormone surge

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

Perinatal androgen exposure decreases the size of the sexually dimorphic medial preoptic nucleus in the rat.

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