2011-01-012024-05-14https://scholars.lib.ntu.edu.tw/handle/123456789/660154摘要：脊髓背角的活化是造成神經痛的重要中樞 (central sensitizeation) 過敏機制，神經損傷後如何造成脊髓背角之活化，進而行程神經痛，其分子機制並不清楚。本計畫假設神經損傷後，熱休克蛋白(HSP) 的增加及其磷酸化與脊髓背角之活化有關。將以慢性狹窄型損傷與 resiniferatoxin 所致之神經病變為模式，探討於背根神經節與脊髓背角之熱休克蛋白之表達，以及相關轉錄因子造成疼痛分子之表達與神經疼痛行為。研究結果將可以對神經痛之脊髓背角機制提供新的資訊與治療策略。<br> Abstract: Dorsal horn is the major gate of central sensitization in injury-induced neuropathic pain. The mechanisms underlying the links between nerve injury and molecular signatures of neuropathic pain, however, remain obscured. In this proposal, we will explore the role of small heat shock protein (HSP) in the pathogenesisof injury-induced neuropathic pain. We hypothesize that nerve injury will induce the expression of HSP in dorsal root ganglia (DRG) neurons, which will lead to the activation of transcription factors, molecular pain mediators and neuropathic pain behaviors. In this proposal, we will employ chronic constrictioninjury and resiniferatoxin-induced neuropathy as models to investigate these molecular cascades. We will examine the expression of HSP and its phosphorylated form in the dorsal horn and DRG neurons and then silence the expression of HSP with antisense oligonucleotide. The findings will shed on the mechanisms and potential therapeutic strategies of injury-induced neuropathic pain.神經痛神經病變神經退化neuropathic painneuropathyneurodegeneration