Changes in magnesium concentration in the serum and cerebrospinal fluid of neuropathic rats
Changes in magnesium concentration in the serum and cerebrospinal fluid of neuropathic rats
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DOI：
10.1111/j.1399-6576.2006.00925.x
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发表时间：
2006-02-01
影响因子：
2.1
通讯作者：
Han, SM
中科院分区：
文献类型：
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作者：
Jeong, SM;Hahm, KD;Han, SM
神经性疼痛的中枢致敏与细胞外钙通过n -甲基-d-天冬氨酸（NMDA）受体控制的离子通道的开放流入有关，这些离子通道通常被镁栓阻断。由于缺镁大鼠出现机械性痛觉过敏，鞘内或腹腔内注射镁可抑制神经性疼痛，因此神经性疼痛时血清和脑脊液中镁的浓度可能发生改变。因此，我们比较了神经病变大鼠与无神经性疼痛症状的损伤大鼠和正常大鼠血清和脑脊液中镁的浓度。采用左腰椎第5、第6脊神经紧密结扎的方法，对雄性Sprague-Dawley大鼠进行机械异常性痛的诱导。在第3天、第7天和第14天，采用von Frey丝刺激下的戒断反应，采用上下法评估足爪戒断阈值。选取阈值小于4 g的大鼠作为有症状组，与无症状组、未手术对照组和假手术组进行比较。第16天测定血清和脑脊液中Mg2+的浓度。有症状的神经病大鼠血清和脑脊液中镁的浓度与无症状神经性疼痛的损伤大鼠、假手术大鼠和正常大鼠无明显差异。我们的研究结果表明，尽管NMDA受体控制的离子通道被激活，但通过血脑屏障的主动转运维持了生理稳态。然而，神经性疼痛的大鼠可能在效应部位处于缺镁状态，因此镁治疗可以减轻神经性疼痛。
Central sensitization of neuropathic pain is associated with an influx of extracellular calcium via the opening of N-methyl-d-aspartate (NMDA) receptor-gated ion channels, which are usually blocked by magnesium plugs. As magnesium-deficient rats develop a mechanical hyperalgesia and intrathecal or intraperitoneal magnesium suppresses neuropathic pain, the magnesium concentrations in serum and cerebrospinal fluid may be altered in neuropathic pain. We therefore compared the magnesium concentrations in serum and cerebrospinal fluid of neuropathic rats with those in injured rats without symptoms of neuropathic pain and normal rats.Mechanical allodynia was induced in male Sprague-Dawley rats by tight ligature of the left lumbar fifth and sixth spinal nerves. The threshold of paw withdrawal was evaluated by the up-down method using withdrawal response to stimulus with a von Frey filament on the third, seventh and 14th days. Rats with a threshold of less than 4 g were selected as the symptomatic group and compared with an asymptomatic group, an unoperated control group and a sham-operated group. On the 16th day, the Mg2+ concentrations in serum and cerebrospinal fluid were measured.The magnesium concentrations in the serum and cerebrospinal fluid of symptomatic neuropathic rats did not differ from those in the injured rats without symptoms of neuropathic pain, sham-operated rats and normal rats.Our results suggest that physiologic homeostasis is maintained by active transport through the blood-brain barrier despite the activation of NMDA receptor-gated ion channels. However, rats with neuropathic pain may be in a magnesium-deficient condition at the effector site, such that magnesium treatment can decrease neuropathic pain.