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本文引用的文献

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Fragile X mental retardation protein regulates the levels of scaffold proteins and glutamate receptors in postsynaptic densities.脆性X智力低下蛋白调节突触后致密物中支架蛋白和谷氨酸受体的水平。
J Biol Chem. 2009 Sep 18;284(38):25479-87. doi: 10.1074/jbc.M109.042663. Epub 2009 Jul 28.
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Roles of mGluR5 in synaptic function and plasticity of the mouse thalamocortical pathway.代谢型谷氨酸受体5(mGluR5)在小鼠丘脑皮质通路突触功能和可塑性中的作用
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mGluR5 regulates glutamate-dependent development of the mouse somatosensory cortex.代谢型谷氨酸受体5(mGluR5)调节小鼠体感皮层依赖谷氨酸的发育。
J Neurosci. 2008 Dec 3;28(49):13028-37. doi: 10.1523/JNEUROSCI.2600-08.2008.
4
Cortical adenylyl cyclase 1 is required for thalamocortical synapse maturation and aspects of layer IV barrel development.皮质腺苷酸环化酶1是丘脑皮质突触成熟和IV层桶状结构发育所必需的。
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Circuit and plasticity defects in the developing somatosensory cortex of FMR1 knock-out mice.脆性X智力低下基因1敲除小鼠发育中的体感皮层的回路和可塑性缺陷
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Glutamate transporters regulate lesion-induced plasticity in the developing somatosensory cortex.谷氨酸转运体调节发育中的体感皮层损伤诱导的可塑性。
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Developmental trajectories and correlates of sensory processing in young boys with fragile X syndrome.脆性X综合征男童的感觉加工发育轨迹及其相关因素
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Fragile X syndrome.脆性X综合征
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Neuron. 2007 Dec 20;56(6):955-62. doi: 10.1016/j.neuron.2007.12.001.
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The functional organization of the barrel cortex.桶状皮层的功能组织。
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FMR1 基因敲除小鼠的桶状皮层中,关键期可塑性被破坏。

Critical period plasticity is disrupted in the barrel cortex of FMR1 knockout mice.

机构信息

Department of Physiology, Northwestern University Feinberg School of Medicine, 303 E Chicago Avenue, Chicago, IL 60611, USA.

出版信息

Neuron. 2010 Feb 11;65(3):385-98. doi: 10.1016/j.neuron.2010.01.024.

DOI:10.1016/j.neuron.2010.01.024
PMID:20159451
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2825250/
Abstract

Alterations in sensory processing constitute prominent symptoms of fragile X syndrome; however, little is known about how disrupted synaptic and circuit development in sensory cortex contributes to these deficits. To investigate how the loss of fragile X mental retardation protein (FMRP) impacts the development of cortical synapses, we examined excitatory thalamocortical synapses in somatosensory cortex during the perinatal critical period in Fmr1 knockout mice. FMRP ablation resulted in dysregulation of glutamatergic signaling maturation. The fraction of silent synapses persisting to later developmental times was increased; there was a temporal delay in the window for synaptic plasticity, while other forms of developmental plasticity were not altered in Fmr1 knockout mice. Our results indicate that FMRP is required for the normal developmental progression of synaptic maturation, and loss of this important RNA binding protein impacts the timing of the critical period for layer IV synaptic plasticity.

摘要

感觉处理的改变构成了脆性 X 综合征的突出症状;然而,对于感觉皮层中突触和回路发育的破坏如何导致这些缺陷知之甚少。为了研究脆性 X 智力迟钝蛋白 (FMRP) 的缺失如何影响皮质突触的发育,我们在 Fmr1 敲除小鼠的感觉皮层围产期关键期检查了兴奋性丘脑皮质突触。FMRP 缺失导致谷氨酸能信号转导成熟失调。持续到后期发育时间的沉默突触比例增加;突触可塑性的窗口存在时间延迟,而 Fmr1 敲除小鼠的其他形式的发育可塑性没有改变。我们的结果表明,FMRP 是突触成熟正常发育进程所必需的,这种重要的 RNA 结合蛋白的缺失会影响 IV 层突触可塑性的关键期的时间。