Assessment of spinal cord chemokine signaling in the mechanism of neuropathic pain.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25460721
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Pain science
• Research Institution: Kyushu University
• Principal Investigator: Saitoh Hidetoshi 九州大学, 薬学研究科(研究院), 准教授 (90444794)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 神経障害性疼痛 / ミクログリア / ケモカイン

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.

Free Research Field

神経薬理学