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配对联想刺激对主动肌-拮抗肌代表区皮质可塑性的影响。

Effects of Paired Associative Stimulation on Cortical Plasticity in Agonist-Antagonist Muscle Representations.

作者信息

Suzuki Makoto, Saito Kazuo, Maeda Yusuke, Cho Kilchoon, Iso Naoki, Okabe Takuhiro, Suzuki Takako, Yamamoto Junichi

机构信息

Faculty of Health Sciences, Tokyo Kasei University, 2-15-1 Inariyama, Sayama City 350-1398, Saitama, Japan.

Faculty of Systems Design, Tokyo Metropolitan University, 1-1 Minami-Osawa, Hachioji City 192-0397, Tokyo, Japan.

出版信息

Brain Sci. 2023 Mar 10;13(3):475. doi: 10.3390/brainsci13030475.

DOI:10.3390/brainsci13030475
PMID:36979285
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10046224/
Abstract

Paired associative stimulation (PAS) increases and decreases cortical excitability in primary motor cortex (M1) neurons, depending on the spike timing-dependent plasticity, i.e., long-term potentiation (LTP)- and long-term depression (LTD)-like plasticity, respectively. However, how PAS affects the cortical circuits for the agonist and antagonist muscles of M1 is unclear. Here, we investigated the changes in the LTP- and LTD-like plasticity for agonist and antagonist muscles during PAS: 200 pairs of 0.25-Hz peripheral electric stimulation of the right median nerve at the wrist, followed by a transcranial magnetic stimulation of the left M1 with an interstimulus interval of 25 ms (PAS-25 ms) and 10 ms (PAS-10 ms). The unconditioned motor evoked potential amplitudes of the agonist muscles were larger after PAS-25 ms than after PAS-10 ms, while those of the antagonist muscles were smaller after PAS-25 ms than after PAS-10 ms. The γ-aminobutyric acid A (GABA)- and GABA-mediated cortical inhibition for the agonist and antagonist muscles were higher after PAS-25 ms than after PAS-10 ms. The cortical excitability for the agonist and antagonist muscles reciprocally and topographically increased and decreased after PAS, respectively; however, GABA and GABA-mediated cortical inhibitory functions for the agonist and antagonist muscles were less topographically decreased after PAS-10 ms. Thus, PAS-25 ms and PAS-10 ms differentially affect the LTP- and LTD-like plasticity in agonist and antagonist muscles.

摘要

配对联想刺激(PAS)可增加或降低初级运动皮层(M1)神经元的皮层兴奋性,这分别取决于尖峰时间依赖性可塑性,即长时程增强(LTP)样可塑性和长时程抑制(LTD)样可塑性。然而,PAS如何影响M1的主动肌和拮抗肌的皮层回路尚不清楚。在此,我们研究了PAS期间主动肌和拮抗肌的LTP样和LTD样可塑性的变化:对腕部右侧正中神经进行200对0.25Hz的外周电刺激,随后以25ms(PAS-25ms)和10ms(PAS-10ms)的刺激间隔对左侧M1进行经颅磁刺激。PAS-25ms后主动肌的非条件运动诱发电位幅度大于PAS-10ms后,而PAS-25ms后拮抗肌的非条件运动诱发电位幅度小于PAS-10ms后。PAS-25ms后主动肌和拮抗肌的γ-氨基丁酸A(GABA)及GABA介导的皮层抑制作用高于PAS-10ms后。PAS后,主动肌和拮抗肌的皮层兴奋性分别呈相互对应且按拓扑结构增加和降低;然而,PAS-10ms后,主动肌和拮抗肌的GABA及GABA介导的皮层抑制功能在拓扑结构上降低较少。因此,PAS-25ms和PAS-10ms对主动肌和拮抗肌的LTP样和LTD样可塑性有不同影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e84e/10046224/971b6676d480/brainsci-13-00475-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e84e/10046224/4f4945660265/brainsci-13-00475-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e84e/10046224/1b4cac6a875c/brainsci-13-00475-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e84e/10046224/a572ffa39913/brainsci-13-00475-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e84e/10046224/971b6676d480/brainsci-13-00475-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e84e/10046224/4f4945660265/brainsci-13-00475-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e84e/10046224/1b4cac6a875c/brainsci-13-00475-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e84e/10046224/a572ffa39913/brainsci-13-00475-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e84e/10046224/971b6676d480/brainsci-13-00475-g004.jpg

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