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Extremely low frequency magnetic field induces hyperalgesia in mice modulated by nitric oxide synthesis.

机译:极低频磁场在由一氧化氮合成调节的小鼠中诱发痛觉过敏。

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We investigated an effect of extremely low frequency magnetic field (ELF-MF, 60 Hz) on hyperalgesia using hot plate test. The level of nitric oxide (NO) and the expression of nitric oxide synthase (NOS) were measured to determine if ELF-MF is engaged in NO mediated pain mechanism. Additionally, the involvement of Ca2+-dependent NO pathway in ELF-MF induced hyperalgesia was evaluated by blocking Ca2+ sources with NMDA receptor antagonist and Ca2+ channel blocker. The exposure of mice to ELF-MF lowered pain threshold and elevated NO synthesis in brain and spinal cord. An NOS inhibitor blocked these effects of ELF-MF with attenuating the reduction of pain threshold and the rise of NO level in brain and spine by the exposure of ELF-MF. The hyperalgesic effects of ELF-MF were also blocked by a Ca2+ channel blocker, nimodipine, but not by a NMDA receptor antagonist, MK-801. The expression of Ca2+ -dependent nNOS and eNOS and Ca2+ -independent iNOS were not changed by ELF-MF. These results indicated that the exposure of ELF-MF might cause Ca2+ -dependent NOS activation, which then induces hyperalgesia with the increase in NO synthesis. In conclusion, ELF-MF may produce hyperalgesia by modulating NO synthesis via Ca2+ -dependent NOS.
机译:我们使用热板试验研究了极低频磁场(ELF-MF,60 Hz)对痛觉过敏的影响。测量一氧化氮(NO)的水平和一氧化氮合酶(NOS)的表达,以确定ELF-MF是否参与NO介导的疼痛机制。另外,通过用NMDA受体拮抗剂和Ca 2+通道阻滞剂阻​​断Ca 2+来源,评估了ELF-MF诱导的痛觉过敏中Ca 2+依赖性NO途径的参与。小鼠暴露于ELF-MF可以降低疼痛阈值,并提高脑和脊髓中的NO合成。 NOS抑制剂通过暴露于ELF-MF来减轻疼痛阈值的降低以及脑部和脊柱中NO水平的升高,从而阻断了ELF-MF的这些作用。 ELF-MF的镇痛作用也被Ca2 +通道阻滞剂尼莫地平阻断,但未被NMDA受体拮抗剂MK-801阻断。依赖Ca2 +的nNOS和eNOS的表达以及不依赖Ca2 +的iNOS的表达不会被ELF-MF改变。这些结果表明,暴露于ELF-MF可能引起Ca2 +依赖性NOS活化,然后随着NO合成的增加而引起痛觉过敏。总之,ELF-MF可能通过依赖于Ca2 +的NOS调节NO合成而产生痛觉过敏。

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