Short-interval paired-pulse inhibition and facilitation of human motor cortex: the dimension of stimulus intensity
Short-interval paired-pulse inhibition and facilitation of human motor cortex: the dimension of stimulus intensity
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DOI：
10.1113/jphysiol.2002.030122
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发表时间：
2002-11-15
影响因子：
5.5
通讯作者：
Ziemann, U
中科院分区：
文献类型：
--
作者：
Ilic, TV;Meintzschel, F;Ziemann, U
经颅配对。磁刺激极大地促进了我们对控制人类运动皮层兴奋性的机制的理解。虽然很明显，成对脉冲兴奋性取决于第一个刺激（S1）和第二个刺激（S2）之间的确切刺激间隔（ISI），但对S1和S2的强度的影响以及通过GABA（A）受体操纵神经传递的影响知之甚少。当记录静息状态下小趾展肌（ADM）的运动诱发电位（MEP）时，采用固定的ISI 1.5ms，并将S1和S2之间的相互作用表示为MEPS 1 +S2/（MEPS 1 + MEPS 2）时，如果S1和S2近似等于MEP阈值（RMT），则S1和S2强度的系统变化显示短间期皮层内易化（SICF），或者如果S1 > RMT且S2 < RMT。相反，如果S1 RMT，则发生短间隔皮质内抑制（SICI）< RMT and S2 >。ADM的收缩使SICT保持不变，但减少了SICF。GABA（A）受体激动剂地西泮增加静息ADM的SICI，减少SICF，而地西泮对ADM收缩无影响。表面肌电图和单运动单位记录显示，在ADM收缩SICI发作是在I3波潜伏期的S2，而SICF通常“跳起来”的一个I波，并开始与I2波潜伏期的S2。结果表明，SICI是通过一个低阈值GABA（A）受体依赖性抑制通路和来自S1的IPSP和来自S2的EPSP在皮质脊髓的总和介导的。神经元相反，SICF起源于中间神经元的起始轴突段的非突触易化，沿着沿着高阈值兴奋通路。
Paired transcranial. magnetic stimulation has greatly advanced our understanding of the mechanisms which control excitability in human motor cortex. While it is clear that paired-pulse excitability depends on the exact interstimulus interval (ISI) between the first (S1) and second stimulus (S2), relatively little is known about the effects of the intensities of S1 and S2, and the effects of manipulating neurotransmission through the GABA(A) receptor. When recording the motor evoked potential (MEP) from the resting abductor digiti minimi (ADM) muscle, using a fixed ISI of 1.5 ms, and expressing the interaction between S1 and S2 as MEPS1+S2/(MEPS1 + MEPS2), then a systematic variation of the intensities of S1 and S2 revealed short-interval intracortical facilitation (SICF) if S1 and S2 were approximately equal to MEP threshold (RMT), or if S1 > RMT and S2 < RMT. In contrast, short-interval intracortical inhibition (SICI) occurred if S1 < RMT and S2 > RMT. Contraction of the ADM left SICT unchanged but reduced SICF. The GABA(A) receptor agonist diazepam increased SICI and reduced SICF in the resting ADM while diazepam had no effect during ADM contraction. Surface EMG and single motor unit recordings revealed that during ADM contraction SICI onset was at the I3-wave latency of S2, whereas SICF typically 'jumped up' by one I-wave and started with the I2-wave latency of S2. Findings suggest that SICI is mediated through a low-threshold GABA(A) receptor-dependent inhibitory pathway and summation of IPSP from S1 and EPSP from S2 at the corticospinal. neurone. In contrast, SICF originates through non-synaptic facilitation at the initial axon segment of interneurones along a high-threshold excitatory pathway.