Division of Neurosciences, Yamaguchi University Graduate School of Medicine, 1-1-1 Minami-Kogushi, Ube, Yamaguchi 755-8505, Japan.
Cell Mol Neurobiol. 2012 Mar;32(2):245-53. doi: 10.1007/s10571-011-9756-4. Epub 2011 Oct 4.
Recent studies have demonstrated that magnetic stimulation (MS) can induce cellular responses such as Ca(2+) influx into the cultured neurons and glia, leading to increased intracellular phosphorylation. We have demonstrated previously that MS reduces rat neuropathic pain associated with the prevention of neuronal degeneration. Thus, we aimed to elucidate the actions of MS in relation to modulation of spinal neuron-glia and the descending inhibitory system in chronic pain. The male SD rats intrathecally implanted with catheters were subjected to sciatic nerve ligation (CCI). MS is a low power apparatus characterized by two different frequencies, 2 KHz and 83 MHz. Rats were given MS to the skin (injured sciatic nerve) for 10 min from the seventh day after CCI. The paw withdrawal latency (PWL) evoked by thermal stimuli was measured for 14 days after CCI. Immunohistochemistry for Iba-1 or GFAP was performed after 4% paraformaldehyde fixation (microscopic analysis). We employed microdialysis for measuring CSF 5-HIAA as a reflection of 5-HT release by MS stimulation. Following CCI, rats showed a decrease in PWL after CCI, and the decrease continued until the 14th day. With MS treatment, the decrease in PWL was reduced during the 10-14 day after CCI. Injection of JNK-1 inhibitors on the 14th day antagonized the analgesic effect of MS. MS also eliminated the CCI-induced decrease in GFAP immunoreactivity. Moreover, MS evoked spinal 5-HT release reflected by increase in spinal 5-HIAA level. Thus, we demonstrate that a novel magnetic stimulator used cutaneously can ameliorate chronic pain by not only preventing abnormal spinal neuron-glia interaction, but also through the activation of the supra-spinal descending inhibitory system.
最近的研究表明，磁刺激（MS）可以诱导细胞反应，如培养神经元和神经胶质细胞中的 Ca(2+)内流，导致细胞内磷酸化增加。我们之前已经证明，MS 可以减轻与神经元变性预防相关的大鼠神经性疼痛。因此，我们旨在阐明 MS 在调节慢性疼痛中的脊髓神经元-神经胶质和下行抑制系统中的作用。鞘内置管的雄性 SD 大鼠接受坐骨神经结扎（CCI）。MS 是一种低功率仪器，具有两种不同的频率，2 KHz 和 83 MHz。CCI 后第 7 天开始，MS 对皮肤（损伤的坐骨神经）进行 10 分钟治疗。CCI 后 14 天测量热刺激引起的足底回缩潜伏期（PWL）。CCI 后 4%多聚甲醛固定后进行 Iba-1 或 GFAP 免疫组织化学（显微镜分析）。我们采用微透析法测量 CSF 5-HIAA，以反映 MS 刺激对 5-HT 释放的影响。CCI 后，大鼠 PWL 在 CCI 后下降，并且这种下降持续到第 14 天。MS 治疗后，CCI 后第 10-14 天 PWL 的下降减少。CCI 后第 14 天注射 JNK-1 抑制剂拮抗 MS 的镇痛作用。MS 还消除了 CCI 引起的 GFAP 免疫反应性降低。此外，MS 诱发的脊髓 5-HT 释放反映在脊髓 5-HIAA 水平的增加。因此，我们证明了一种新的经皮使用的磁刺激器不仅可以通过防止异常的脊髓神经元-神经胶质相互作用，而且可以通过激活脊髓上的下行抑制系统来改善慢性疼痛。
