Circuit and plasticity defects in the developing somatosensory cortex of Fmr1 knock-out mice
Circuit and plasticity defects in the developing somatosensory cortex of Fmr1 knock-out mice
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DOI：
10.1523/jneurosci.1076-08.2008
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发表时间：
2008-05-14
影响因子：
5.3
通讯作者：
Svoboda, Karel
中科院分区：
文献类型：
--
作者：
Bureau, Ingrid;Shepherd, Gordon M. G.;Svoboda, Karel
Fmr1 基因沉默会导致脆性 X 综合征。尽管大脑皮层突触可塑性缺陷与 Fmr1 敲除 (ko) 小鼠的认知障碍有关，但该综合征影响的具体皮层回路尚不清楚。在这里，我们研究了 Fmr1 ko 小鼠桶状皮层兴奋性投射的发展。在 2 周大的 Fmr1 ko 小鼠中，连接第 4 层 (L4) 到 L3 (L43L3) 的主要上升突起存在多种独立的缺陷：由于连接概率较低，其强度降低； L4细胞的轴突乔木在L2/3中空间分散； L43L3 投影没有表现出依赖于经验的可塑性。 3 周时，L43L3 投射的强度与野生型相似。我们的数据表明，Fmr1 在发育关键期塑造感觉皮层回路。
Silencing of the Fmr1 gene causes fragile X syndrome. Although defects in synaptic plasticity in the cerebral cortex have been linked to cognitive impairments in Fmr1 knock-out (ko) mice, the specific cortical circuits affected in the syndrome are unknown. Here, we investigated the development of excitatory projections in the barrel cortex of Fmr1 ko mice. In 2-week-old Fmr1 ko mice, a major ascending projection connecting layer 4 (L4) to L3 (L43L3), was defective in multiple and independent ways: its strength was reduced, caused by a lower connection probability; the axonal arbors of L4 cells were spatially diffuse in L2/3; the L43L3 projection did not show experience-dependent plasticity. By 3 weeks, the strength of the L43L3 projection was similar to that of wild type. Our data indicate that Fmr1 shapes sensory cortical circuits during a developmental critical period.