2014 Fiscal Year Final Research Report
The molecular mechanism of anti-allodynic effect of GDNF in the rat neuropathic pain model
Project/Area Number |
24590737
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Pain science
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Research Institution | Hyogo Medical University |
Principal Investigator |
FUKUOKA Tetsuo 兵庫医科大学, 医学部, 非常勤講師 (90399147)
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Project Period (FY) |
2012-04-01 – 2015-03-31
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Keywords | GDNF / BDNF / NPY / 機械的知覚過敏 / ナトリウムチャネル / 神経障害性疼痛 / 後索核 |
Outline of Final Research Achievements |
We investigated the molecular mechanisms of mechanical allodynia using the rat L5 spinal nerve ligation model. Following peripheral nerve damage, the injured heavily myelinated primary afferent neurons up-regulated BDNF and NPY expression. Our data suggested that these neuropeptides were released in the ipsilateral gracile nucleus by spontaneous firing of these neurons and facilitated touch sense processing causing mechanical allodynia. Additionally, we found that muscle-innervating primary afferent neurons normally lacked Nav1.7, an alpha-subunit of voltage-gated sodium channel, but began to express this channel following nerve injury. Nav1.7 may exert an important role for spontaneous firing.
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Free Research Field |
神経障害性疼痛の分子メカニズム
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