| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Outline of Final Research Achievements |
Lysophosphatidic acid (LPA) signaling initiates the molecular machineries of neuropathic pain. At the level of spinal cord, LPA also plays key roles in the amplification of initial pain signals and possibly in the maintenance of pain. On the other hand, endocannabinoids (ECs) such as anandamide or 2-arachidonoylglycerol (2-AG) are known to play roles in the suppression of inflammatory or nociceptive pain signal through CB1 receptor on primary afferent sensory fibers as another type of reverse signals. In this study, we discovered that LPA increased the gene expression of the degradation of ECs and the decreased the ECs level. This counter-balancing cross-talk system between LPA and ECs is differently regulated in the neuropathic and inflammatory pain. These results are important for understanding of the machinery between acute and chronic pain and drug discovery.
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