Epigenetics analysis in abnormal behavior through dopamin receptors
| Project/Area Number |
21890281
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Biological pharmacy
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| Research Institution | Ritsumeikan University |
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Principal Investigator |
INDEN Masatoshi Ritsumeikan University, 薬学部, 助教 (70512424)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥2,652,000 (Direct Cost: ¥2,040,000、Indirect Cost: ¥612,000)
Fiscal Year 2010: ¥1,261,000 (Direct Cost: ¥970,000、Indirect Cost: ¥291,000)
Fiscal Year 2009: ¥1,391,000 (Direct Cost: ¥1,070,000、Indirect Cost: ¥321,000)
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| Keywords | パーキンソン病 / ドパミン神経 / セロトニン神経 / 6-hydroxydopamine / フルオキセチン / L-dopa / リン酸化ヒストンH3 / 線条体 |
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| Research Abstract |
In this study, we demonstrated that pre-treatment with fluoxetine, an SSRIs, significantly suppressed L-DOPA-induced ERK1/2 and histone H3 phosphorylation, as well as L-DOPA-induced rotational behavior in 6-OHDA-lesioned rats. These data indicate that L-DOPA-derived DA, released as a "false transmitter" from 5-HT terminals, enhances levels of phosphorylated ERK and histone H3, and this results in abnormal behavior. Fluoxetine may attenuate these effects of a false transmitter via 5-HT receptor. In further support of this supposition, these effects of fluoxetine were abolished by pre-treatment with WAY 100135, a 5-HT1A antagonist.
These results suggest that fluoxetine may influence motor function in PD via pharmacological modification of interactions between serotonergic and dopaminergic neuronal networks.
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Report
(3 results)
Research Products
(12 results)
