کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
915683 1473263 2006 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Mitochondrial electron transport in models of neuropathic and inflammatory pain
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب سلولی و مولکولی
پیش نمایش صفحه اول مقاله
Mitochondrial electron transport in models of neuropathic and inflammatory pain
چکیده انگلیسی

Although peripheral nerve function is strongly dependent on energy stores, the role of the mitochondrial electron transport chain, which drives ATP synthesis, in peripheral pain mechanisms, has not been examined. In models of HIV/AIDS therapy (dideoxycytidine), cancer chemotherapy (vincristine), and diabetes (streptozotocin)-induced neuropathy, inhibitors of mitochondrial electron transport chain complexes I, II, III, IV, and V significantly attenuated neuropathic pain-related behavior in rats. While inhibitors of all five complexes also attenuated tumor necrosis factor α-induced hyperalgesia, they had no effect on hyperalgesia induced by prostaglandin E2 and epinephrine. Two competitive inhibitors of ATP-dependent mechanisms, adenosine 5′-(β,γ-imido) triphosphate and P1,P4-di(adenosine-5′) tetraphosphate, attenuated dideoxycytidine, vincristine, and streptozotocin-induced hyperalgesia. Neither of these inhibitors, however, affected tumor necrosis factor α, prostaglandin E2 or epinephrine hyperalgesia. These experiments demonstrate a role of the mitochondrial electron transport chain in neuropathic and some forms of inflammatory pain. The contribution of the mitochondrial electron transport chain in neuropathic pain is ATP dependent.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Pain - Volume 121, Issues 1–2, March 2006, Pages 105–114
نویسندگان
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