Repetitive transcranial magnetic stimulation induced analgesia depends on N-methyl-D-aspartate glutamate receptors
Repetitive transcranial magnetic stimulation induced analgesia depends on N-methyl-D-aspartate glutamate receptors
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DOI：
10.1016/j.pain.2013.12.022
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发表时间：
2014-03-01
期刊：
影响因子：
7.4
通讯作者：
Bouhassira, Didier
中科院分区：
文献类型：
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作者：
de Andrade, Daniel Ciampi;Mhalla, Alaa;Bouhassira, Didier
本研究探讨了谷氨酸N-甲基-D-天冬氨酸（NMDA）受体在重复经颅磁刺激（rTMS）镇痛效应中的作用。在一项随机、双盲、交叉研究中，我们比较了氯胺酮和安慰剂对运动皮层（M1）或背外侧前额叶皮层/运动前皮层（DLPFC/PMC）刺激镇痛作用的影响。三组12名健康志愿者在间隔2周的2个实验期间接受右侧M1的主动rTMS（10 Hz，80%静息运动阈值，每次1，500个脉冲）、右侧DLPFC/PMC的主动刺激或假刺激。分别于刺激前及刺激后1h在左侧鱼际隆起测定冷痛阈，评价rTMS的镇痛作用。在皮层刺激期间静脉内给予氯胺酮（0.15 mg/kg，10分钟推注，随后以6 lg/kg/分钟持续输注，直至rTMS结束）或安慰剂（盐水）。我们还系统地测量了治疗前后的皮质兴奋性参数（静息运动阈值，阈上运动诱发电位，短皮层内抑制和皮层内易化），以研究皮质兴奋性变化与rTMS诱导的镇痛之间的可能关系。氯胺酮注射显著降低M1和DLPFC/PMC刺激的镇痛作用。rTMS的镇痛作用的减少与皮质兴奋性参数的变化无关，而皮质兴奋性参数在给予生理盐水或氯胺酮后不受rTMS的影响。因此，rTMS诱导的镇痛依赖于谷氨酸NMDA受体，并可能涉及长时程增强样机制。(C)2013年国际疼痛研究协会。Elsevier B. V.出版，保留所有权利。
We investigated the role of glutamate N-methyl-D-aspartate (NMDA) receptors in the analgesic effects induced by repetitive transcranial magnetic stimulation (rTMS). In a randomized, double-blind, crossover study, we compared the effects of ketamine and placebo on the analgesic effects of motor cortex (M1) or dorsolateral prefrontal cortex/premotor cortex (DLPFC/PMC) stimulation. Three groups of 12 healthy volunteers underwent active rTMS (10 Hz, 80% resting motor threshold, 1,500 pulses per session) of the right M1, active stimulation of the right DLPFC/PMC, or sham stimulation during 2 experimental sessions 2 weeks apart. Cold pain thresholds were measured on the left thenar eminence before and 1 hour after cortical stimulation, to evaluate the analgesic effects of rTMS. Ketamine (0.15 mg/kg in a 10-minute bolus followed by continuous infusion of 6 lg/kg per minute until the end of rTMS) or placebo (saline) were administered intravenously during cortical stimulation. We also systematically measured cortical excitability parameters (resting motor threshold, suprathreshold motor-evoked potentials, short intracortical inhibition, and intracortical facilitation) before and after treatment, to investigate the possible relationship between changes in cortical excitability and rTMS-induced analgesia. Ketamine injection significantly decreased the analgesic effects of both M1 and DLPFC/PMC stimulation. The decrease in the analgesic effect of rTMS was not associated with changes in cortical excitability parameters, which were not influenced by rTMS following the administration of either saline or ketamine. Thus, rTMS-induced analgesia depends on glutamate NMDA receptors and may involve long-term potentiation-like mechanisms. (C) 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.