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本文引用的文献

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Transient and persistent dendritic spines in the neocortex in vivo.体内新皮层中短暂和持久的树突棘
Neuron. 2005 Jan 20;45(2):279-91. doi: 10.1016/j.neuron.2005.01.003.
2
Dendritic spine dynamics are regulated by monocular deprivation and extracellular matrix degradation.树突棘动力学受单眼剥夺和细胞外基质降解的调节。
Neuron. 2004 Dec 16;44(6):1021-30. doi: 10.1016/j.neuron.2004.12.001.
3
Dendritic spines disappear with chilling but proliferate excessively upon rewarming of mature hippocampus.树突棘在成熟海马体冷却时消失,但在复温后过度增殖。
Neuroscience. 2004;127(1):69-80. doi: 10.1016/j.neuroscience.2004.04.053.
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What have genetically engineered mice taught us about ischemic injury?基因工程小鼠让我们对缺血性损伤有了哪些了解?
Curr Mol Med. 2004 Mar;4(2):207-25. doi: 10.2174/1566524043479194.
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Tissue microenvironments within functional cortical subdivisions adjacent to focal stroke.与局灶性中风相邻的功能性皮质亚区内的组织微环境。
J Cereb Blood Flow Metab. 2003 Sep;23(9):997-1009. doi: 10.1097/01.WCB.0000084252.20114.BE.
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Biochemistry of ischemic stroke.缺血性中风的生物化学
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Plasticity of cortical projections after stroke.中风后皮质投射的可塑性。
Neuroscientist. 2003 Feb;9(1):64-75. doi: 10.1177/1073858402239592.
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Long-term dendritic spine stability in the adult cortex.成年皮质中树突棘的长期稳定性。
Nature. 2002;420(6917):812-6. doi: 10.1038/nature01276.
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Long-term in vivo imaging of experience-dependent synaptic plasticity in adult cortex.成年皮质中经验依赖性突触可塑性的长期体内成像
Nature. 2002;420(6917):788-94. doi: 10.1038/nature01273.
10
Experience-dependent changes in dendritic arbor and spine density in neocortex vary qualitatively with age and sex.新皮层中树突分支和棘密度的经验依赖性变化在质量上随年龄和性别而有所不同。
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体内树突棘结构的快速可逆变化受缺血程度控制。

Rapid reversible changes in dendritic spine structure in vivo gated by the degree of ischemia.

作者信息

Zhang Shengxiang, Boyd Jamie, Delaney Kerry, Murphy Timothy H

机构信息

Kinsmen Laboratory, Department of Psychiatry, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3.

出版信息

J Neurosci. 2005 Jun 1;25(22):5333-8. doi: 10.1523/JNEUROSCI.1085-05.2005.

DOI:10.1523/JNEUROSCI.1085-05.2005
PMID:15930381
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6724996/
Abstract

Current therapeutic windows for effective application of thrombolytic agents are within 3-6 h of stroke. Although treatment can improve outcome, it is unclear what happens to synaptic fine structure during this critical period in vivo. The relationship between microcirculation and dendritic spine structure was determined in mouse somatosensory neurons during stroke. Spines were, on average, 13 mum from a capillary and were supplied by approximately 100 red blood cells per second. Moderate ischemia (approximately 50% supply) did not significantly affect spines within 5 h; however, severe ischemia (<10% supply) caused a rapid loss of spine and dendrite structure within as little as 10 min. Surprisingly, if reperfusion occurred within 20-60 min, dendrite and spine structure was mostly restored. These data suggest that the basic dendritic wiring diagram remains mostly intact during moderate ischemia and that affected synapses could potentially contribute to functional recovery. With severe ischemia, markedly deformed dendritic structure can partially recover if reperfusion occurs early.

摘要

目前溶栓药物有效应用的治疗窗是在中风后的3 - 6小时内。尽管治疗可以改善预后,但在此关键的体内时期突触精细结构会发生什么尚不清楚。在中风期间,研究了小鼠体感神经元中微循环与树突棘结构之间的关系。树突棘平均距离毛细血管13微米,每秒约有100个红细胞供应。中度缺血(约50%的供血)在5小时内不会对树突棘产生显著影响;然而,严重缺血(供血<10%)在短短10分钟内就会导致树突棘和树突结构迅速丧失。令人惊讶的是,如果在20 - 60分钟内发生再灌注,树突和树突棘结构大多会恢复。这些数据表明,在中度缺血期间基本的树突布线图大多保持完整,并且受影响的突触可能有助于功能恢复。在严重缺血时,如果早期发生再灌注,明显变形的树突结构可以部分恢复。