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本文引用的文献

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Interactions between ICAM-5 and β1 integrins regulate neuronal synapse formation.细胞间黏附分子-5 与β1 整合素相互作用调节神经元突触形成。
J Cell Sci. 2013 Jan 1;126(Pt 1):77-89. doi: 10.1242/jcs.106674. Epub 2012 Sep 26.
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Compensatory redistribution of neuroligins and N-cadherin following deletion of synaptic β1-integrin.突触β1 整合素缺失后神经黏附素和 N 钙黏蛋白的代偿性再分布。
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Effects of aging and sensory loss on glial cells in mouse visual and auditory cortices.衰老和感觉丧失对小鼠视觉和听觉皮层神经胶质细胞的影响。
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HIV-1 Tat-induced microgliosis and synaptic damage via interactions between peripheral and central myeloid cells.HIV-1 Tat 通过外周和中枢髓样细胞之间的相互作用诱导小胶质细胞增生和突触损伤。
PLoS One. 2011;6(9):e23915. doi: 10.1371/journal.pone.0023915. Epub 2011 Sep 2.
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Influence of matrix metalloproteinase MMP-9 on dendritic spine morphology.基质金属蛋白酶 MMP-9 对树突棘形态的影响。
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Methamphetamine-associated cleavage of the synaptic adhesion molecule intercellular adhesion molecule-5.甲基苯丙胺导致细胞间黏附分子 5 突触黏附分子的裂解。
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Microglial interactions with synapses are modulated by visual experience.小胶质细胞与突触的相互作用受视觉经验的调节。
PLoS Biol. 2010 Nov 2;8(11):e1000527. doi: 10.1371/journal.pbio.1000527.
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Preparation of mouse brain tissue for immunoelectron microscopy.用于免疫电子显微镜的小鼠脑组织制备。
J Vis Exp. 2010 Jul 20(41):2021. doi: 10.3791/2021.
9
EphA4 is localized in clathrin-coated and synaptic vesicles in adult mouse brain.EphA4 在成年老鼠大脑中的网格蛋白包被囊泡和突触小泡中定位。
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10
Matrix metalloproteinase-dependent shedding of intercellular adhesion molecule-5 occurs with long-term potentiation.细胞间黏附分子-5 的基质金属蛋白酶依赖性脱落与长时程增强有关。
Neuroscience. 2010 Mar 17;166(2):508-21. doi: 10.1016/j.neuroscience.2009.12.061. Epub 2010 Jan 4.

在缺乏基质金属蛋白酶-9的情况下,视觉皮层中细胞间粘附分子5(端脑连蛋白)的亚细胞定位不受发育调控。

Subcellular localization of intercellular adhesion molecule-5 (telencephalin) in the visual cortex is not developmentally regulated in the absence of matrix metalloproteinase-9.

作者信息

Kelly Emily A, Tremblay Marie-Eve, Gahmberg Carl G, Tian Li, Majewska Ania K

机构信息

Department of Neurobiology and Anatomy, University of Rochester, Rochester, New York, 14642.

出版信息

J Comp Neurol. 2014 Feb 15;522(3):676-88. doi: 10.1002/cne.23440.

DOI:10.1002/cne.23440
PMID:23897576
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3877171/
Abstract

The telencephalon-associated intercellular adhesion molecule-5 (telencephalin; ICAM-5) regulates dendritic morphology in the developing brain. In vitro studies have shown that ICAM-5 is found predominantly within dendrites and immature dendritic protrusions, with reduced expression in mushroom spines, suggesting that ICAM-5 downregulation is critical for the maturation of synaptic structures. However, developmental expression of ICAM-5 has not been explored in depth at the ultrastructural level in intact brain tissue. To investigate the ultrastructural localization of ICAM-5 with transmission electron microscopy, we performed immunoperoxidase histochemistry for ICAM-5 in mouse visual cortex at postnatal day (P)14, a period of intense synaptogenesis, and at P28, when synapses mature. We observed the expected ICAM-5 expression in dendritic protrusions and shafts at both P14 and P28. ICAM-5 expression in these dendritic protrusions decreased in prevalence with developmental age to become localized predominantly to dendritic shafts by P28. To understand better the relationship between ICAM-5 and the endopeptidase metalloproteinase-9 (MMP-9), which mediates ICAM-5 cleavage following glutamate activation during postnatal development, we also explored ICAM-5 expression in MMP-9 null animals. This analysis revealed a similar expression of ICAM-5 in dendritic elements at P14 and P28; however, an increased prevalence of ICAM-5 was noted in dendritic protrusions at P28 in the MMP-9 null animals, indicating that, in the absence of MMP-9, there is no developmental shift in ICAM-5 subcellular localization. Our ultrastructural observations shed light on possible functions mediated by ICAM-5 and their regulation by extracellular proteases.

摘要

端脑相关细胞间黏附分子5(端脑素;ICAM - 5)在发育中的大脑中调节树突形态。体外研究表明,ICAM - 5主要存在于树突和未成熟的树突状突起中,在蘑菇状棘中的表达减少,这表明ICAM - 5的下调对于突触结构的成熟至关重要。然而,在完整脑组织的超微结构水平上,尚未深入研究ICAM - 5的发育表达。为了通过透射电子显微镜研究ICAM - 5的超微结构定位,我们在出生后第14天(P14)和P28(突触成熟时)对小鼠视觉皮层进行了ICAM - 5的免疫过氧化物酶组织化学检测。我们在P14和P28时均观察到树突状突起和树突干中有预期的ICAM - 5表达。随着发育年龄的增长,这些树突状突起中ICAM - 5的表达普遍性降低,到P28时主要定位于树突干。为了更好地理解ICAM - 5与内肽酶金属蛋白酶9(MMP - 9)之间的关系,MMP - 9在出生后发育过程中在谷氨酸激活后介导ICAM - 5的裂解,我们还研究了MMP - 9基因敲除动物中ICAM - 5的表达。该分析显示,在P14和P28时,树突成分中ICAM - 5的表达相似;然而,在MMP - 9基因敲除动物的P28树突状突起中,ICAM - 5的表达普遍性增加,这表明在没有MMP - 9的情况下,ICAM - 5亚细胞定位没有发育性转变。我们的超微结构观察揭示了ICAM - 5介导的可能功能及其受细胞外蛋白酶调节的情况。