| Project/Area Number |
15390555
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Okayama University |
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Principal Investigator |
SUGIMOTO Tomosada Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Professor, 大学院医歯薬学総合研究科, 教授 (50135729)
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| Co-Investigator(Kenkyū-buntansha) |
ICHIKAWA hiroyuki Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Associate Professor, 大学院医歯薬学総合研究科, 助教授 (20193435)
YAMAAI yuichiro Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Research Associate, 大学院医歯薬学総合研究科, 助手 (00158057)
TERAYAMA ryuji Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Research Associate, 大学院医歯薬学総合研究科, 助手 (60333689)
FUJITA masako Okayama University, Dental School, Research Assistant, 歯学部, 教務員 (40156881)
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| Project Period (FY) |
2003 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥12,900,000 (Direct Cost: ¥12,900,000)
Fiscal Year 2006: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2005: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2004: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2003: ¥9,300,000 (Direct Cost: ¥9,300,000)
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| Keywords | dorsal root ganglion / primary neuron / apoptosis / TUNEL / caspase-3 / caspase-9 / caspase-8 / pain / 三叉神経節 / カプサイシン / 脊髄後根神経節 / 無髄線維 / IB4 / saporin / 侵害受容 / 細胞死 / 細胞毒 / 神経切断 / 3次ニューロン |
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| Research Abstract |
Sensory primary neurons of newborn rats are vulnerable to apoptotic cell death induced by various kinds of insults. To explore a possibility that the neonatal injury-induced cell death is conducted by a caspase-dependent mechanism, two types of animal models of peripheral injury were delivered to newborn rats ; i. e, systemic administration of capsaicin (50 mg/kg, s.c.), and transection of the infraorbital or sciatic nerve. At various post-injury intervals, the rats were killed and the trigeminal (TG) and dorsal root ganglia (DRG) were processed for immunohistochemistry for activated caspase-9,-8,-3 or TUNEL for DNA fragmentation.
Neonatal capsaicin administration induced caspase-immunoreactivity (ir) and DNA fragmentation in neuronal cell bodies in the TG and DRG. Starting at 16h post-injury the immunoreactive (ir) and TUNEL-positive TG and DRG neurons increased, reached the peak at 24h, and then decreased. Double-stain analysis at 24h indicated the co-expression of DNA fragmentation w
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ith caspase-9-ir or caspase-3-ir. Comparison of two adjacent sections immunostained for the two different antigens revealed co-expression of the two caspases.
Nerve transection induced caspase-3-ir and DNA fragmentation in neuronal cell bodies in the corresponding ganglion ipsilateral to the injury. The temporal distribution patterns of caspase-3-ir and TUNEL-positive neurons were similar to those following capsaicin. The nerve injury significantly induced caspase-9-ir in the maxillary division of the ipsilateral TG at 24h post-injury. Co-expression of caspase-3-ir and DNA fragmentation was also evident following the nerve injury. Following sciatic nerve injury, caspase-8-ir was also examined. Relatively small but significant increase in number of caspase-8-ir neurons was observed.
The present study indicated that systemic capsaicin and peripheral nerve transection in newborn rats induced serial activation of caspases-9 and-3 in the affected sensory primary neurons. Such caspase cascade culminated in DNA fragmentation. Activation of caspase-8 is also involved in the primary neuronal apoptosis following paripheral nerve transection. Less
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