| Project/Area Number |
24590739
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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 |
Pain science
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| Research Institution | Kitasato University (2013-2014)
National Institute for Physiological Sciences (2012) |
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Principal Investigator |
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| Research Collaborator |
YAMAGUCHI Junya
NAKAHATA Yoshihisa
ETO Kei
ISHIKAWA Tatsuya
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 生理学 / 神経科学 / 慢性疼痛 / ＧＡＢＡ / 神経回路 / 大脳皮質 / パッチクランプ法 / 穿孔パッチ法 / 抑制性シナプス後電流 / 慢性痛 / 穿孔パッチクランプ / 細胞内クロライド濃度 / 穿孔パッチクランプ法 |
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| Outline of Final Research Achievements |
Previous studies indicate that plastic changes in the brain likely contribute to chronic pain syndrome. However, its mechanism remained to be clarified. In the present study, we investigated the excitatory and inhibitory synaptic transmission in the primary somatosensory cortex (S1) under chronic pain conditions. We also studied the functional properties of inhibitory neurotransmitter GABA. Excitatory synaptic transmission in the S1 were enhanced in the chronic pain model. Thus activities of not only excitatory but also inhibitory neurons were increased in the S1. On the other hand, a reduction in the function of the potassium-chloride cotransporter, KCC2, occurred during chronic pain, which reduces the efficacy of the inhibitory outputs onto the L2/3 excitatory neurons. Thus, the present results suggest that, the GABA-mediated inhibition is insufficient to completely counterbalance the increased excitation and alleviate the symptoms of chronic pain.
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