University College London, Institute of Neurology, London WC1n 3BG, United Kingdom, University of Heidelberg, Medical Faculty Mannheim, Central Institute of Mental Health, 68159 Mannheim, Germany,
University of Mannheim, School of Social Sciences, 68131 Mannheim, Germany, and.
J Neurosci. 2014 May 21;34(21):7375-82. doi: 10.1523/JNEUROSCI.5139-13.2014.
Prolonged limb immobilization deprives sensorimotor cortical areas of an important source of excitatory input, as well as of motor output. Previous work has described effects on motor excitability but it is unclear whether motor plasticity is also influenced. In two groups of eight healthy human subjects, the left hand was immobilized for 8 h to induce sensorimotor deprivation of the cortical representation of the abductor pollicis brevis muscle. We used transcranial magnetic stimulation protocols to evaluate motor excitability with motor-evoked potentials, input-output (IOcurve) and short-latency intracortical inhibition (SICI) recruitment curves, as well as long-term potentiation (LTP)/long-term depression (LTD)-like plasticity with paired-associative stimulation (PAS) of the median nerve and motor cortex using an interstimulus interval of 25 ms (PAS25) or 10 ms (PAS10), respectively, in two sessions at least 7 d apart (baseline and after immobilization). After immobilization, the slope of the IOcurve decreased, and SICI at lower conditioning pulse intensities was reduced. The LTP-like effects of PAS25 and the LTD-like effect of PAS10 were both significantly enhanced. The effects differed among individuals: the more IOslope decreased after immobilization, the greater the increase of PAS25 and the smaller the increase of PAS10 effects. We suggest that sensorimotor deprivation has two effects. It increases the sensitivity to remaining sensory inputs and therefore increases the effectiveness of both PAS protocols. In addition, it reduces neuronal excitability to an individually different level, as reflected in the reduced IOslope and leads to an interdependent modulation of synaptic plasticity as such as it shifts the threshold of LTP/LTD-like plasticity induction.
长时间的肢体固定会剥夺感觉运动皮层区域重要的兴奋性输入源,以及运动输出。先前的研究描述了对运动兴奋性的影响,但尚不清楚运动可塑性是否也受到影响。在两组 8 名健康的人类受试者中,左手被固定 8 小时,以诱导拇短展肌皮质代表区的感觉运动剥夺。我们使用经颅磁刺激方案通过运动诱发电位、输入-输出(IO 曲线)和短潜伏期皮质内抑制(SICI)募集曲线来评估运动兴奋性,以及使用分别为 25 ms(PAS25)和 10 ms(PAS10)的刺激间隔的正中神经和运动皮层的成对关联刺激(PAS)来评估长时程增强(LTP)/长时程抑制(LTD)样可塑性,两次刺激间隔至少 7 天(基线和固定后)。固定后,IO 曲线的斜率下降,较低的刺激脉冲强度下的 SICI 降低。PAS25 的 LTP 样作用和 PAS10 的 LTD 样作用均显著增强。这些影响在个体之间有所不同:固定后 IO 斜率下降越大,PAS25 的增加越大,PAS10 的增加越小。我们认为感觉运动剥夺有两种作用。它增加了对剩余感觉输入的敏感性,因此增强了两种 PAS 方案的有效性。此外,它将神经元兴奋性降低到个体不同的水平,如 IO 斜率降低所示,并导致作为其改变 LTP/LTD 样可塑性诱导阈值的突触可塑性的相互依赖调节。