Microcircuit mechanisms involved in paired associative stimulation‐induced depression of corticospinal excitability
Microcircuit mechanisms involved in paired associative stimulation‐induced depression of corticospinal excitability
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配对联想刺激引起的皮质脊髓兴奋性抑制的微电路机制
DOI：
10.1113/jphysiol.2013.253989
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发表时间：
2013
期刊：
影响因子：
--
通讯作者：
Jost-Julian
中科院分区：
文献类型：
--
作者：
Ridding;Michael;Eskandar;Martin;Jost-Julian
关键点·将外周神经刺激与相应对侧运动皮层的经颅磁刺激以10 ms重复配对（配对联想刺激; PAS 10），可在短时间窗内对皮质脊髓兴奋性产生中枢效应。·PAS 10诱导的中枢突触效应是由于主要皮质神经元之间的兴奋性突触减弱，但不是位于皮质脊髓神经元上的那些突触或抑制性突触。抑制性中间神经元是产生中枢PAS效应的守门人。同样的机制似乎也控制着PAS 10诱导的周围易化效应。我们提出了一个模型，指定的PAS诱导的可塑性，可能会提高其效用作为一个模型的spike-timing-dependent plasticityinhuman.AbstractSynaptic重量的变化引起的前突触和突触后神经元的尖峰之间的时间相关性所涉及的微电路的组成和层状位置被称为spike-timing-dependent plasticity（STDP）。经颅磁刺激（TMS）如果以短时间间隔与来自相应对侧手部区域的传入刺激重复配对（配对联想刺激，PAS），则会对皮质脊髓兴奋性产生持久影响。PAS诱导的可塑性与突触STDP有关。我们的目的是研究皮质微电路的哪些元素维持和管理PAS诱导的靶肌肉代表中皮质脊髓兴奋性的抑制（以及其功能周围兴奋性的增强）。我们发现，两种刺激诱导的皮层事件之间的相互作用导致立即干预后抑郁的时间窗很短（<4.5 ms）。通过在主TMS脉冲之前3 ms施加亚阈值磁脉冲，即使调整主TMS脉冲的强度以产生与非条件磁脉冲类似幅度的运动诱发电位，也可完全阻断目标表征处的MPAS效应。患者颈髓的硬膜外记录显示，在这种情况下，晚期TMS诱发的I波仍然受到抑制。当PAS过程中TMS成分的强度降低时-足以激活抑制性神经元，但不足以激活皮质脊髓神经元-短潜伏期皮质内抑制的兴奋性保持不变。PAS诱导的功能周围的易化遵循与中枢效应相同的模式。这些发现可能表明，兴奋性-PAS-诱导的效应是由于上皮层主神经元之间的兴奋性突触减弱，而不是位于皮质脊髓神经元或抑制性突触上的突触。参与短潜伏期皮质内抑制的抑制性中间神经元是产生中枢/周围易化PAS效应的守门人。基于这些和早期的研究结果，我们提出了一个模型，该模型指定了PAS诱导的可塑性所涉及的微电路的组成和层位置，这可能会增强其作为人类STDP模型的实用性。
Key points•Repetitively pairing peripheral nerve stimulation with transcranial magnetic stimulation of the corresponding contralateral motor cortex at 10 ms (paired associative stimulation; PAS10) leads to centre‐depressant effects on corticospinal excitability in a short time window.•PAS10‐induced centre‐depressant effects are due to weakening of excitatory synapses between principal cortical neurons, but not those located on corticospinal neurons, or inhibitory synapses.•Inhibitory interneurons are gate‐keepers to producing centre‐depressant PAS effects. The same mechanisms appear to govern PAS10‐induced surround‐facilitatory effects.•We propose a model specifying the composition and laminar location of the involved microcircuit of PAS‐induced plasticity that may enhance its utility as a model of spike‐timing‐ dependent plasticity in humans.AbstractSynaptic weight changes induced by temporal correlations between the spikes of pre‐ and postsynaptic neurons are referred to as spike‐timing‐dependent plasticity (STDP). Transcranial magnetic stimulation (TMS) induces long‐lasting effects on corticospinal excitability, if it is repetitively paired with stimulation of afferents from a corresponding contralateral hand region at short intervals (paired associative stimulation, PAS). PAS‐induced plasticity has been linked with synaptic STDP. We aimed to investigate which elements of the cortical microcircuitry sustain and govern PAS‐induced depression of corticospinal excitability in the target muscle representation (and enhancement of excitability in its functional surround). We show that the time window during which the interaction between both stimulus‐induced cortical events leads to immediate post‐interventional depression is short (<4.5 ms). The depressant PAS effects at the target representation were completely blocked by applying a subthreshold magnetic pulse 3 ms before the principal TMS pulse, even when the strength of the latter was adjusted to generate a motor‐evoked potential of similar amplitude to that with the unconditioned magnetic pulse. Epidural recordings from the cervical cord of a patient showed that under this condition late TMS‐evoked I‐waves remain suppressed. When the intensity of the TMS component during PAS was lowered – sufficient to allow activation of inhibitory neurons, but insufficient to activate corticospinal neurons – excitability of short‐latency intracortical inhibition remained unchanged. PAS‐induced facilitation in the functional surround followed the same pattern as the centre‐depressant effects. These findings may suggest that excitability‐depressant PAS‐induced effects are due to weakening of excitatory synapses between upper cortical layer principal neurons, but not those located on the corticospinal neuron, or inhibitory synapses. Inhibitory interneurons involved in short‐latency intracortical inhibition are gate‐keepers to producing centre‐depressant/surround‐facilitatory PAS effects. Based on these and earlier findings we propose a model specifying the composition and laminar location of the involved microcircuit of PAS‐induced plasticity that may enhance its utility as a model of STDP in humans.
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劳拉西泮对人运动皮层兴奋性的影响
影响因子：
2
作者：
U. Ziemann;S. Lönnecker;B. Steinhoff;W. Paulus
通讯作者：
W. Paulus
影响因子：
2
作者：
Di Lazzaro, Vincenzo;Dileone, M.;Tonali, P. A.
通讯作者：
Tonali, P. A.
影响因子：
2.5
作者：
Born, RT
通讯作者：
Born, RT
DOI：
--
发表时间：
1986
期刊：
Journal de physiologie
影响因子：
--
作者：
H. Wigström;B. Gustafsson
通讯作者：
H. Wigström;B. Gustafsson
影响因子：
2
作者：
Heide, G.;Witte, O. W.;Ziemann, U.
通讯作者：
Ziemann, U.