中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/26729
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    題名: 探討電針刺激調控尿禁制與其在脊髓上的相關機制
    其他題名: Investigation of Acupuncture Modulates Continence and Relationship with Spinal Cord Mechanism
    作者: 林則彬(Tzer-Bin Lin);陳進典;陳漢明
    貢獻者: 醫學院醫學系學士班生理學科
    日期: 2010-08-31
    上傳時間: 2010-09-09 11:47:59 (UTC+8)
    摘要: 給予環磷醯胺 (cyclophosphamide, CYP) 造成膀胱的骨盆傳入神經敏感化，因此誘發恥骨上疼痛 (suprapubic pain)。探討 CYP 可能藉由增加脊髓活化造成的神經朔性改變，進而導致內臟性疼痛。比較 Veh 處理和CYP處理的老鼠之間，骨盆神經-尿道反射活性和脊髓上 NR2B 次單元磷酸化的變化。當給予 CYP 較Veh 處理，造成反覆性電刺激所誘導的脊髓反射增益效應增加，伴隨腰薦部 (L6-S2) 的脊髓背角上磷酸化 NR2B 次單元的表現量增加。此外，當給予 NOS 或 Cdk5 拮抗劑 (L-NAME; roscovitine)，可逆轉 CYP 所增加的反射增益效應和 NR2B 次單元磷酸化的現象。利用 NR2B 次單元的 siRNA，降低 NR2B 次單元的表現量，阻斷 CYP 依賴性的反射活性以及脊髓上NR2B 次單元的磷酸化。此結果證實 CYP 經由 NO 和 Cdk5 依賴性 NR2B 次單元的磷酸化，調控脊髓上的 NMDA 接受器產生反射增益效應，此現象可以參與了內臟性疼痛的發生。

    It is well-established that cyclophosphamide (CYP) can sensitize the pelvic afferent nerve arising from the urinary bladder, and therefore, induce suprapubic pain. To test the possibility that CYP might facilitate spinal activity-dependent neural plasticity to mediate the development of visceral hypereflexia/hyperalgesia, we compared pelvic-urethra reflex activity and spinal NR2B phosphorylation in vehicle solution (Veh)- and CYP-treated rats. In accompanied with up-regulation of phosphorylated NR2B expression in lumbosacral (L6-S2) dorsal horn, CYP facilitated repetitive stimulation (1 stimulation/ 1 sec)-induced spinal reflex potentiation by increasing the evoked spikes when compared with vehicle solution. Moreover, the facilitation of reflex potentiation and NR2B phosphorylation caused by CYP were reversed both by L-NAME and roscovitine, NOS and Cdk5 antagonists respectively. When compared with negative control, Si-RNA of NR2B, which decreased the expression of NR2B expression, abolished CYP-dependent reflex facilitation and spinal NR2B phosphorylation. These results suggested that CYP might facilitate spinal N-methyl-D-aspartate receptors (NMDARs)-mediated reflex potentiation to participate in the development of visceral hypereflexia/hyperalgesia through NO- and Cdk5-dependent NR2B phosphorylation at lumbosacral dorsal horn.
    顯示於類別:[醫學系] 研究計畫

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