| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Research Abstract |
We investigated the change of glial cells and neurons in spinal cord (SC) using two neuropathic pain models, partial sciatic nerve ligation (PSNL) mice and streptozotocin (STZ)-induced diabetic mice. In PSNL mice, microglia increased on the ligation side of the SC, but not neurons. Astrocytes also tended to increase on the ligation side of the SC. In diabetic mice, microglia, astrocytes and neurons were not changed in the SC. Next, Minocycline, a microglial inhibitor, was administrated daily before and after PSNL, or only after PSNL in PSNL mice. The administration of Minocycline before and after PSNL prevented not only the increase of microglia and astrocytes, also allodynia induced by nerve ligation at 7 days. The results suggest that spinal microglia and astrocytes contribute to the development in neuropathic pain in PSNL model, but not diabetic model. It is highly possible the cure of PSNL-induced allodynia if we are able to inhibited microglial proliferation in SC after PSNL. In PSNL model, there was no significant difference the amplitude and the frequency of miniature inhibitory postsynaptic currents (mIPSC) between the ipsilateral and the contralateral side of II/III and V layer of the anterior cingulated cortex (ACC). In diabetic mice, the frequency of mIPSC tended to decrease in II/III layer of ACC compared with vehicle group, but not significantly change. These results show that it may have a little influence on inhibitory responses in ACC in PSNL model and STZ model.
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