Mechanism of deficit in sexual behavior of metabotropic glutamate receptor subtype 7 knockout mice
Project/Area Number |
20500313
|
Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Nerve anatomy/Neuropathology
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Research Institution | Kyoto Prefectural University of Medicine |
Principal Investigator |
TOKITA Miwako Kyoto Prefectural University of Medicine, 医学研究科, 助教 (10420712)
|
Co-Investigator(Kenkyū-buntansha) |
SAKAMOTO Hirotaka 岡山大学, 大学院・自然科学研究科, 准教授 (20363971)
|
Project Period (FY) |
2008 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | 神経微細形態学 / 性行動 / 分子神経生物学 / グルタミン酸 / mGluR7 / 攻撃行動 / 社会的行動 / mGluR |
Research Abstract |
We examined the sexual behavior in male wild-type and metabotropic glutamate receptor subtype 7 knockout mice (mGluR7 KO) littermates. Wefound that mGluR7 KO has difficulty in ejaculation. Furthermore, we also examined the aggressive behavior of these mice, using a resident-intruder paradigm. Wild-type micedisplayed intense aggression against olfactory bulbectomized intruders. In comparison, mGluR7 KO showed significantly reduced levels of aggression. mGluR7 KO showedreduced plasma testosterone level. Castration reduced both sexual and aggressive behavior to equivalent low levels in both wild type and mGluR7 KO. Testosterone replacement restored these behaviors to pre-castration levels in both genotypes.
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Report
(4 results)
Research Products
(12 results)