演題番号 : P1-p07
大西 新 / Arata Oh-Nishi:1 永井 裕司 / Yuji Nagai:1 須原 哲也 / Tetsuya Suhara:1 大林 茂 / Shigeru Obayashi:1
1:（独）放射線医学総合研究所 分子神経イメージング研究グループ / Molecular Neuroimaging Group, National Institute of Radiological Sciences.
Major mental disorders such as schizophrenia are characterized by disturbances of thoughts, perception, cognition and volition. It is reported that about 1% of the world population becomes morbid with schizophrenia. However, the schizophrenia pathology and onset mechanism are not well known. Recently, it was reported that dopamine D2 receptor (D2R) binding decreases in the medial prefrontal cortex (mPFC) in schizophrenia patients (Suhara et al 2002). On the other hand, it has been indicated that maternal immune activation increases the risk of psychiatric disorders such as schizophrenia in offspring. This suggests the possibility that maternal immune activation induces disruption of the dopaminergic system, which then leads to schizophrenia pathology in offspring. To test this hypothesis, we gave Toll-like receptor3 ligand synthetic double-stranded RNA polyriboinosinic-polyribocytidilic acid (Poly I:C) (0.4mg/kg/day), which mimics viral infection causing immune activation, to pregnant rats on gestation days 15-18. Then we investigated D2R ligand (C11-labeled FLB457) binding potential in whole brain of mature offspring of Poly I:C-treated dams by positron emission tomography. We found that C11-labeled FLB457 binding potential significantly decreased in mPFC in mature offspring of Poly I:C-treated dams (P<0.05). This result indicates a high degree of homology between the animal model of schizophrenia with maternal immune activation and schizophrenia patients, in terms of disruption of the dopaminergic system. We suggest that maternal immune activation might evoke schizophrenia-like pathology in adulthood.