| Project/Area Number |
23592173
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NAKATSUKA Terumasa 関西医療大学, 保健医療学部, 客員教授 (30380752)
TANIGUCHI Wataru 関西医療大学, 保健医療学部, 准教授 (20453194)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | シグナル伝達 / ROS / パッチクランプ法 / TRPA1 / TRPV1 / 脊髄損傷後疼痛 / 活性酸素種 / 脊髄後角 / スカベンジャー / 疼痛増強 / 脊髄損傷 / 脊髄膠様質 / 神経障害性疼痛 / フリーラジカル / ＲＯＳ / in vivo パッチクランプ法 |
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| Research Abstract |
Reactive oxygen species (ROS) have been recognized to play an important role in central neuropathic pain (CNP) in the spinal cord, such as chronic pain after spinal cord injury (SCI). To clarify how ROS impact on excitatory synaptic transmission, we investigated the effects of ROS on synaptic transmission in rat spinal cord substantia gelatinosa (SG) neurons using whole-cell patch-clamp recordings. Administration of t-BOOH, an ROS donor, into the spinal cord markedly increased the frequency and amplitude of spontaneous excitatory postsynaptic currents (sEPSCs) in SG neurons. Moreover, in the presence of a TRPA1 or TRPV1 channel antagonist, the t-BOOH-induced increase in the frequency of sEPSCs was inhibited. These results indicate that the excessive activation of TRPA1 and TRPV1 channels by ROS may induce central sensitization in the spinal cord and result in chronic pain such as that following SCI.
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