2015 Fiscal Year Final Research Report
Elucidating the mechanism of the effects of N-acetyl cysteine on animal models of mental disorders
| Project/Area Number |
26860920
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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 |
Psychiatric science
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Keywords | 精神疾患 / 細胞内システィン / シスチン-グルタミン酸交換体 / タンパク質翻訳系 / タンパク質分解系 / 依存症 / 神経可塑性 |
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| Outline of Final Research Achievements |
It was predicted that protein synthesis would be attenuated in the nucleus accumbent (NAc) of chronic cocaine-treated rats due to intracellular cysteine shortage -induced attenuation of thiolation of tRNA which resulted from dysfunction of cystine-glutamate anti porter (xCT). However, the existence of MOCS3, which is supposed to catalyst tRNA violation, was not confirmed. In addition, the amount of total glutathione, which demands cysteine for its synthesis, was not affected by cocaine, Another intracellular cysteine supplying pathway from methionine owing to the enzymatic activity of cystathionine beta synthase was also less likely, because its activity was not altered by cocaine. Thus, it is concluded that intracellular cysteine was supplied by unknown pathway besides via xCT, and the basel levels of protein synthesis was not affected in the NAc by repeated cocaine treatment. On the other hand , N-acteyl-cysteine robustly promoted protein degradation in chronic cocaine-treated rats.
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| Free Research Field |
神経薬理学
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