| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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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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