2012 Fiscal Year Final Research Report
How are trace amines involved in pathophysiology of schizophrenia ?
| 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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| Keywords | trace amine / schizophrenia / aromatic L-amino acid decarboxylase / dopamine / mesolimbic system / TAAR1 / D-neuron |
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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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[Remarks] つばめ会会報
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[Remarks] 磐城共立病院医報
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