| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Outline of Final Research Achievements |
Neuropathic pain is a debilitating pain state, which is often caused by injury to the nervous system. Hallmark symptoms of neuropathic pain include tactile allodynia and thermal hyperalgesia, which are refractory to currently available treatments such as non-steroidal anti-inflammatory drugs and opioids. The mechanism underlying development of neuropathic pain remains largely unknown. Therefore, unraveling the molecular and cellular basis of the development and maintenance of neuropathic pain is essential for the discovery of new treatments.
In this study, we reported that upregulation of CCL3 and CCR5 was induced in the spinal cord after nerve injury, and that the CCR5 antagonist can alleviate neuropathic pain.Further more, in primary cultured microglia,we found that P2Y12 receptor activation induced CCL3 expression via NFAT signaling.
These results suggest that CCL3-CCR5 axis is crucial in the mechanism of neuropathic pain, and CCR5 might be a therapeutic target for neuropathic pain.
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