| Project/Area Number |
23790295
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General pharmacology
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| Research Institution | Osaka University |
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Principal Investigator |
HAYATA Atsuko 大阪大学, 連合小児発達学研究科, 助教 (70390812)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 受容体 / シグナル情報伝達系 / PACAP / 神経細胞 / 樹状突起スパイン / 精神疾患 / 5-HT 2A受容体 / インターナリゼーション / FRET / 5-HT2 |
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| Research Abstract |
In this study, we showed that the number of PSD-95-labeled synaptic puncta was decreased in primary cultured hippocampal neurons prepared from PACAP-/- mice while it was increased by PACAP in the neurons from wild-type mice, and PACAP increased miR-132 expression and decreased mRNA and protein expression levels of p250GAP which is involved in dendritic spine formation and targeted by miR-132.PACAP induced 5-HT2A receptor internalization in a dose-and time-dependent manner. VIP did not induce 5-HT2A receptor internalization, suggesting that PAC1 is involved in the PACAP-induced 5-HT2A receptor internalization. In addition, we observed that pretreatment with the protein kinase C (PKC) inhibitor sphingosineinhibited the 5-HT2A receptor internalization.
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