| Project/Area Number | 08660342 |
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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, School of Agricultural Sciences, Assistant Professor, 農学部, 助手 (00212051)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed(Fiscal Year 1997)
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| Budget Amount *help |
¥2,400,000 (Direct Cost : ¥2,400,000)
Fiscal Year 1997 : ¥1,000,000 (Direct Cost : ¥1,000,000)
Fiscal Year 1996 : ¥1,400,000 (Direct Cost : ¥1,400,000)
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| Keywords | luteinizing hormone / fasting stress / estrogen / estrogen receptor / A2 region of solitary tract nucleus / paraventricular nucleus / noradrenergic neurons / 延髄孤束核A2領域 / ノルアドレナリン作働性神経 |
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| Research Abstract |
Fasting-stress profoundly suppresses luteinizing hormone (LH) secretion in the rat in a estrogen dependent manner. It has been demonstrated that this suppression is mediated by noradrenergic neurons projecting to the hypothalamic paraventricular nucleus (PVN). The present research aimed to investigate further brain mechanism mediating the fasting-induced suppression of LH release.
Forty-eight h fasting significantly increased numbers of estrogen receptor-containing cells in both the PVN and A2 region of solitary tract nucleus (NTS) in the lower brain stem. Acute infusion of estrogen into the PVN caused an inhibition of pulsatile LH release only in the 48-h fasted ovariectomized (OVX) rats, but not in the ad lib-fed OVX rats. On the other hand, the estrogen infusion into the NTS did not affect LH secretion. The estrogen infusion into the both nuclei did not affect the noradrenaline release in the PVN.These results suggest that fasting induces estrogen receptor expression in the PVN where estrogen acts to suppresses LH secretion without affecting noradrenaline release.
It has demonstrated that intravenous injection of 2-deoxyglucose (2DG), a glucose antagonist, suppressed pulsatile LH release in OVX rats in a dose-dependent manner and that estrogen enhanced the inhibitory effect of 2DG on LH pulses. Furthermore, 2DG induced noradrenaline release in the PVN,and local injection of catecholamine synthesis inhibitor into the PVN blocked 2DG-induced suppression of LH secretion. These results suggest that suppression of LH release by lowered glucose availability is mediated y noradrenergic neurons projecting the PVN.
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