| Project/Area Number |
22591265
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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 |
Psychiatric science
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
IKEMOTO Keiko 福島県立医科大学, 医学部, 研究員 (90184449)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | trace amine / schizophrenia / aromatic L-amino acid decarboxylase / dopamine / mesolimbic system / TAAR1 / D-neuron / 芳香族アミノ酸脱炭酸酵素 / ドパミン / 中脳辺縁系 / 統合失調症 / D-ニューロン / 神経幹細胞 / トレースアミン / ドーパミン / トレースアミン関連受容体1型(TAAR1) / 免疫組織化学 / 死後脳 / β-フェニルエチルアミン |
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| Research Abstract |
“D-cell hypothesis” of schizophrenia was proposed. Our previous studies have shown D-neuron reduction in the striatum, notably in nucleus accumbens in postmortem brains of patients with schizophrenia. The localization of subvebtricular zone NSC, being overlapped with that of striatal D-neurons, lead to suspect that striatalD-neuron decrease would be caused by NSC hypofunction. Striatal TA decrease may decrease TAAR1 stimulation on nerve terminals of VTA DA neurons, which would result in midbrain DA hyperactivity in schizophrenia. Dopamine D2 receptorstimulation onto striatal NSC may cause NCS hypofunction, and acceleration ofD-neuron reduction and mesolimbic DA hyperactivity of schizophrenia. This is in agreement with effectiveness of early intervention by DA D2 blocker for first episode schizophrenia, and also with prospectiveness of TAAR1 agonists as novel antipsychotics.
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