| Budget Amount *help |
¥12,740,000 (Direct Cost: ¥9,800,000、Indirect Cost: ¥2,940,000)
Fiscal Year 2017: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2014: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
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| Outline of Final Research Achievements |
In this research, we first clarified that the intrinsic neuronal excitability of ventral tegmental area (VTA) dopaminergic neurons projecting to the nucleus accumbens (N.Acc.) was significantly reduced in neuropathic pain- and cancer pain-model mice using patch clamp electrophysiology. Under these conditions, we found that phasic activation of mesolimbic dopaminergic neurons produced a significant but transient anti-allodynic effect in these mice using optogenetics or designer receptors exclusively activated by designer drugs (DREADD) technology. On the other hand, we revealed that the expression of Dnmt3a was significantly increased along with the downregulation of miR-200b/429 expression in the N.Acc. under the neuropathic pain condition. Furthermore, we found that a significant decrease in Pde10a expression in the N.Acc. was caused by an increase in the level of DNA methylation at the Pde10a promoter.
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