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首页> 外文期刊>Neuron >Critical period plasticity is disrupted in the barrel cortex of FMR1 knockout mice.
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Critical period plasticity is disrupted in the barrel cortex of FMR1 knockout mice.

机译：关键期可塑性在FMR1基因敲除小鼠的桶状皮质中被破坏。

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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.
机译：感觉过程的改变构成脆性X综合征的突出症状。然而，关于感觉皮层中突触和电路发育受阻如何导致这些缺陷的了解甚少。若要调查脆弱的X智力低下蛋白（FMRP）的损失如何影响皮层突触的发展，我们检查了围产期关键期Fmr1基因敲除小鼠体内感觉皮层的兴奋性丘脑皮层突触。 FMRP消融导致谷氨酸能信号传导成熟失调。沉默突触的比例持续到以后的发育时间增加。 Fmr1基因敲除小鼠中突触可塑性的窗口有时间延迟，而其他形式的发育可塑性没有改变。我们的结果表明，FMRP是突触成熟的正常发育过程所必需的，并且这种重要的RNA结合蛋白的丢失会影响IV层突触可塑性的关键时期。

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