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两半球间可塑性是通过最大限度地增强胼胝体传入而介导的。

Interhemispheric plasticity is mediated by maximal potentiation of callosal inputs.

机构信息

Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892;

Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.

出版信息

Proc Natl Acad Sci U S A. 2019 Mar 26;116(13):6391-6396. doi: 10.1073/pnas.1810132116. Epub 2019 Mar 7.

DOI:10.1073/pnas.1810132116
PMID:30846552
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6442599/
Abstract

Central or peripheral injury causes reorganization of the brain's connections and functions. A striking change observed after unilateral stroke or amputation is a recruitment of bilateral cortical responses to sensation or movement of the unaffected peripheral area. The mechanisms underlying this phenomenon are described in a mouse model of unilateral whisker deprivation. Stimulation of intact whiskers yields a bilateral blood-oxygen-level-dependent fMRI response in somatosensory barrel cortex. Whole-cell electrophysiology demonstrated that the intact barrel cortex selectively strengthens callosal synapses to layer 5 neurons in the deprived cortex. These synapses have larger AMPA receptor- and NMDA receptor-mediated events. These factors contribute to a maximally potentiated callosal synapse. This potentiation occludes long-term potentiation, which could be rescued, to some extent, with prior long-term depression induction. Excitability and excitation/inhibition balance were altered in a manner consistent with cell-specific callosal changes and support a shift in the overall state of the cortex. This is a demonstration of a cell-specific, synaptic mechanism underlying interhemispheric cortical reorganization.

摘要

中枢或外周损伤导致大脑连接和功能的重组。在单侧中风或截肢后观察到的一个显著变化是,对未受影响的外周区域的感觉或运动的双侧皮质反应的募集。在单侧胡须剥夺的小鼠模型中描述了这种现象的机制。刺激完整的胡须会在体感桶状皮层中产生双侧血氧水平依赖性 fMRI 反应。全细胞电生理学表明,完整的桶状皮层选择性地增强了到剥夺皮层的第 5 层神经元的胼胝体突触。这些突触具有更大的 AMPA 受体和 NMDA 受体介导的事件。这些因素有助于最大程度地增强胼胝体突触。这种增强会阻断长时程增强,而通过预先诱导长时程抑制,可以在一定程度上挽救这种阻断。兴奋性和兴奋/抑制平衡发生改变,与细胞特异性胼胝体变化一致,并支持皮质整体状态的转变。这证明了大脑半球间皮质重组的一种细胞特异性、突触机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda5/6442599/b0bf99c9a400/pnas.1810132116fig06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda5/6442599/8d380b316689/pnas.1810132116fig01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda5/6442599/2b3f737d7f66/pnas.1810132116fig02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda5/6442599/37e42ea59d0d/pnas.1810132116fig03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda5/6442599/7669a39972be/pnas.1810132116fig04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda5/6442599/c8dd007f14f9/pnas.1810132116fig05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda5/6442599/b0bf99c9a400/pnas.1810132116fig06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda5/6442599/8d380b316689/pnas.1810132116fig01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda5/6442599/2b3f737d7f66/pnas.1810132116fig02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda5/6442599/37e42ea59d0d/pnas.1810132116fig03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda5/6442599/7669a39972be/pnas.1810132116fig04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda5/6442599/c8dd007f14f9/pnas.1810132116fig05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dda5/6442599/b0bf99c9a400/pnas.1810132116fig06.jpg

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