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脆性X智力低下基因1敲除小鼠听觉皮层长期增强的稳定失败。

Failed stabilization for long-term potentiation in the auditory cortex of FMR1 knockout mice.

作者信息

Yang Sungchil, Yang Sunggu, Park Jae-Sung, Kirkwood Alfredo, Bao Shaowen

机构信息

Helen Wills Neuroscience Institute, University of California, Berkeley, California, United States of America.

Department of Neuroscience, Johns Hopkins University, Baltimore, Maryland, United States of America.

出版信息

PLoS One. 2014 Aug 12;9(8):e104691. doi: 10.1371/journal.pone.0104691. eCollection 2014.

Abstract

Fragile X syndrome is a developmental disorder that affects sensory systems. A null mutation of the Fragile X Mental Retardation protein 1 (Fmr1) gene in mice has varied effects on developmental plasticity in different sensory systems, including normal barrel cortical plasticity, altered ocular dominance plasticity and grossly impaired auditory frequency map plasticity. The mutation also has different effects on long-term synaptic plasticity in somatosensory and visual cortical neurons, providing insights on how it may differentially affect the sensory systems. Here we present evidence that long-term potentiation (LTP) is impaired in the developing auditory cortex of the Fmr1 knockout (KO) mice. This impairment of synaptic plasticity is consistent with impaired frequency map plasticity in the Fmr1 KO mouse. Together, these results suggest a potential role of LTP in sensory map plasticity during early sensory development.

摘要

脆性X综合征是一种影响感觉系统的发育障碍。小鼠中脆性X智力低下蛋白1(Fmr1)基因的无效突变对不同感觉系统的发育可塑性有不同影响,包括正常的桶状皮质可塑性、改变的眼优势可塑性以及严重受损的听觉频率图谱可塑性。该突变对体感和视觉皮质神经元的长期突触可塑性也有不同影响,这为其如何不同地影响感觉系统提供了见解。在这里,我们提供证据表明,Fmr1基因敲除(KO)小鼠发育中的听觉皮质中的长时程增强(LTP)受损。这种突触可塑性的损害与Fmr1基因敲除小鼠中频率图谱可塑性的损害一致。这些结果共同表明,LTP在早期感觉发育过程中的感觉图谱可塑性中可能发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9b4/4130563/e16f21231981/pone.0104691.g001.jpg

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