| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2009: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2008: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Research Abstract |
Diabetic subjects have the higher prevalence of depressive and anxiety disorders than the general population. I hypothesized that the hyperglycemic state disrupts the emotional function. In this study, I investigated the effect of diabetes on the emotional behavior in mice. In particular, I focused the glutamatergic system in the frontal cortex and amygdala. Streptozotocin-induced diabetic ICR mice and the age-matched vehicle-treated non-diabetic control mice were used in this study. The emotional behavior was assessed by the conditioned fear test and the elevated open-platform test. Diabetic mice demonstrated the marked anxiety-like behaviors in both behavioral tests compared with non-diabetic mice. In the in vivo mouse microdialysis experiment, the extracellular levels of glutamate were not different between diabetic and non-diabetic mice in either the frontal cortex or amygdala. However, the content of glutamate in the frontal cortex was significantly increased in the frontal cortex, but not in the amygdala, of diabetic mice compared with non-diabetic mice. In the immunoblotting, the total protein level of GluR-1 subunit of AMPA receptor was not different between diabetic and non-diabetic mice in the amygdala. On the other hand, the protein levels of GluR1 subunit phosphorylated at Ser-831 and Ser-845 were markedly increased in the amygdala of diabetic mice compared with non-diabetic mice. The bilateral microinjection of NBQX, a specific AMPA receptor antagonist, suppressed the fear stress-elicited freezing behavior in diabetic mice. Based on these findings, I suggest the possibility that
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