2002 Fiscal Year Final Research Report Summary
Brain mechanism by which estrogen enhances fasting-induced suppression of reproductive function
| Project/Area Number |
13660285
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Applied animal science
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| Research Institution | Nagoya University |
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Principal Investigator |
TSUKAMURA Hiroko Nagoya University Graduate School of Agricultural Sciences, 大学院・生命農学研究科, 助教授 (00212051)
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| Project Period (FY) |
2001 – 2002
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| Keywords | Estrogen receptors / glucose availability / hypothalamic paraventricular nucleus / solitary tract nucleus / fasting stress / luteinizing hormone (LH) / noradrenergic neurons / lactation |
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| Research Abstract |
Fasting-stress profoundly suppresses luteinizing hormone (LH) secretion in the rat in an estrogen dependent manner. It has been demonstrated that 48-h fasting significantly increased numbers of estrogen receptor-containing cells in both the hypothalamic paraventricular nucleus (PVN) and A2 region of solitary tract nucleus (NTS) in the lower brain stem. The present research aimed to investigate the brain mechanism by which estrogen enhances fasting-induced suppression of LH secretion.
Changes in the number of estrogen receptor α (ERα) -containing cells by fasting and pharmacological glucoprivation were investigated in the PVN and NTS of ovariectomized rats. It has been also determined that the anatomical relationship of ERα immunoreactivity within tyrosine hydroxylase (TH) -and dopamine-β-hydroxylase (DBH) -ir neurons in the A2 region of the NTS and the PVN. The number of ERα-ir cells significantly increased after 30 h from the onset of fasting in the PVN and NTS compared with the unfasted controls and was sustained until 48 h. Glucoprivation also significantly increased the number of ERα-ir cells in these nuclei. Forty-eight h fasting and glucoprivation significantly increased ERα-containing TH-/DBH-ir cells. In the PVN, most ERα-ir neurons were juxtaposed with TH-and DBH-ir varicosities. These results suggest that ERα is expressed in specific brain regions at a defined time from the onset of fasting, and that lowered glucose utilization might be the key signal mediating this fasting-induced changes in ERα expression. In addition, the anatomical relationship of noradrenergic and ERα-ir neurons in the A2 region and PVN may suggest a role for estrogen in increasing the activity of noradrenergic neurons in the A2 region and the sensitivity of the PVN to noradrenergic input arising from the lower brainstem and thereby augmenting the suppression of LH secretion during fasting.
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[Publications] Reyes,B.A.S., Yamada,S., Estacio,M.A.C., I'Anson,H., Tsukamura,H. and Maeda,K.-I.: "Glucoprivation increases estrogen receptor α immunoreactivity in the brain catecholaminergic neurons in ovariectomized rats"Neuroscience Letters. 299. 109-112 (2001)
Description
「研究成果報告書概要(欧文)」より
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