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本文引用的文献

1
Diabetes impairs cortical plasticity and functional recovery following ischemic stroke.糖尿病可损害缺血性脑卒中后皮质可塑性和功能恢复。
J Neurosci. 2012 Apr 11;32(15):5132-43. doi: 10.1523/JNEUROSCI.5075-11.2012.
2
Cortical excitation and inhibition following focal traumatic brain injury.局灶性创伤性脑损伤后的皮质兴奋和抑制。
J Neurosci. 2011 Oct 5;31(40):14085-94. doi: 10.1523/JNEUROSCI.3572-11.2011.
3
Relationship between touch impairment and brain activation after lesions of subcortical and cortical somatosensory regions.触觉障碍与皮质下和皮质躯体感觉区域损伤后脑激活之间的关系。
Neurorehabil Neural Repair. 2011 Jun;25(5):443-57. doi: 10.1177/1545968310395777. Epub 2011 Mar 7.
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Frequency of discriminative sensory loss in the hand after stroke in a rehabilitation setting.脑卒中后康复环境中手的感觉辨别丧失频率。
J Rehabil Med. 2011 Feb;43(3):257-63. doi: 10.2340/16501977-0662.
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Age dependence of excitatory-inhibitory balance following stroke.中风后兴奋性-抑制性平衡的年龄依赖性。
Neurobiol Aging. 2012 Jul;33(7):1356-63. doi: 10.1016/j.neurobiolaging.2010.11.019. Epub 2011 Jan 22.
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Reducing excessive GABA-mediated tonic inhibition promotes functional recovery after stroke.降低过度的 GABA 介导的紧张性抑制可促进中风后的功能恢复。
Nature. 2010 Nov 11;468(7321):305-9. doi: 10.1038/nature09511. Epub 2010 Nov 3.
7
Number and laminar distribution of neurons in a thalamocortical projection column of rat vibrissal cortex.大鼠触须皮层丘脑皮质投射柱中神经元的数量和层分布。
Cereb Cortex. 2010 Oct;20(10):2277-86. doi: 10.1093/cercor/bhq067. Epub 2010 Jun 9.
8
Focal cortical infarcts alter intrinsic excitability and synaptic excitation in the reticular thalamic nucleus.局灶性皮质梗死改变网状丘脑核的内在兴奋性和突触兴奋。
J Neurosci. 2010 Apr 14;30(15):5465-79. doi: 10.1523/JNEUROSCI.5083-09.2010.
9
Plasticity during stroke recovery: from synapse to behaviour.中风恢复过程中的可塑性:从突触到行为。
Nat Rev Neurosci. 2009 Dec;10(12):861-72. doi: 10.1038/nrn2735. Epub 2009 Nov 4.
10
Imaging rapid redistribution of sensory-evoked depolarization through existing cortical pathways after targeted stroke in mice.在小鼠靶向性中风后,通过现有皮质通路成像感觉诱发性去极化的快速重新分布。
Proc Natl Acad Sci U S A. 2009 Jul 14;106(28):11759-64. doi: 10.1073/pnas.0812695106. Epub 2009 Jul 1.

中风会导致体感皮层中感觉处理的时间保真度长期受损。

Stroke induces long-lasting deficits in the temporal fidelity of sensory processing in the somatosensory cortex.

机构信息

Division of Medical Sciences, University of Victoria, Victoria, British Columbia, Canada.

出版信息

J Cereb Blood Flow Metab. 2013 Jan;33(1):91-6. doi: 10.1038/jcbfm.2012.135. Epub 2012 Sep 19.

DOI:10.1038/jcbfm.2012.135
PMID:22990417
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3597364/
Abstract

Recovery from stroke is rarely complete as humans and experimental animals typically show lingering deficits in sensory function. One explanation for limited recovery could be that rewired cortical networks do not process sensory stimuli with the same temporal precision as they normally would. To examine how well peri-infarct and more distant cortical networks process successive vibro-tactile stimulations of the affected forepaw (a measure of temporal fidelity), we imaged cortical depolarizations with millisecond temporal resolution using voltage-sensitive dyes. In control mice, paired forepaw stimulations (ranging from 50 to 200 milliseconds apart) induced temporally distinct depolarizations in primary forelimb somatosensory (FLS1) cortex, and to a lesser extent in secondary FLS (FLS2) cortex. For mice imaged 3 months after stroke, the first forepaw stimulus reliably evoked a strong depolarization in the surviving region of FLS1 and FLS2 cortex. However, depolarizations to subsequent forepaw stimuli were significantly reduced or completely absent (for stimuli ≤100 milliseconds apart) in the FLS1 cortex, whereas FLS2 responses were relatively unaffected. Our data reveal that stroke induces long-lasting impairments in how well the rewired FLS1 cortex processes temporal aspects of sensory stimuli. Future therapies directed at enhancing the temporal fidelity of cortical circuits may be necessary for achieving full recovery of sensory functions.

摘要

中风后的恢复很少是完全的,因为人类和实验动物通常在感觉功能上仍存在挥之不去的缺陷。恢复受限的一个解释可能是,重新连接的皮质网络在处理感觉刺激时的时间精度与正常情况不同。为了研究梗死周边和更远的皮质网络在处理受影响前脚的连续振动触觉刺激(衡量时间保真度)的能力如何,我们使用电压敏感染料以毫秒级的时间分辨率对皮质去极化进行成像。在对照小鼠中,成对的前脚刺激(间隔从 50 到 200 毫秒不等)在初级前肢体感(FLS1)皮质中引起时间上明显不同的去极化,在次要的 FLS(FLS2)皮质中则较少。对于中风后 3 个月进行成像的小鼠,第一个前脚刺激可靠地在前脚体感(FLS1)和 FLS2 皮质的存活区域中引起强烈的去极化。然而,后续前脚刺激的去极化显著减少或完全缺失(对于间隔≤100 毫秒的刺激),而 FLS2 的反应则相对不受影响。我们的数据表明,中风导致重新连接的 FLS1 皮质处理感觉刺激时间方面的能力长期受损。未来针对增强皮质电路时间保真度的治疗方法可能对于实现感觉功能的完全恢复是必要的。