Nogo Receptor Signaling Restricts Adult Neural Plasticity by Limiting Synaptic AMPA Receptor Delivery.
Nogo Receptor Signaling Restricts Adult Neural Plasticity by Limiting Synaptic AMPA Receptor Delivery.
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DOI：
10.1093/cercor/bhv232
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发表时间：
2016-01
期刊：
影响因子：
--
通讯作者：
Takahashi T
中科院分区：
文献类型：
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作者：
Jitsuki S;Nakajima W;Takemoto K;Sano A;Tada H;Takahashi-Jitsuki A;Takahashi T
经验依赖性可塑性在成人大脑中是有限的，其分子和细胞机制知之甚少。去除髓鞘抑制信号蛋白Nogo受体（NgR 1），恢复成人神经可塑性。在这里，我们发现，在NgR 1缺陷小鼠中，胡须经验驱动的突触α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体（AMPAR）插入桶皮质，通常在出生后2周完成，持续到成年。双光子显微镜活体成像显示，NgR 1缺陷的成年桶皮质的棘表面上的AMPAR比野生型（WT）小鼠的更多。此外，我们观察到，晶须刺激产生新的棘在成年桶皮质的突变体，但不是野生型小鼠，和新合成的棘含有表面AMPAR。这些结果表明，Nogo信号通过限制突触AMPAR传递与解剖可塑性协调来限制可塑性。
Experience-dependent plasticity is limited in the adult brain, and its molecular and cellular mechanisms are poorly understood. Removal of the myelin-inhibiting signaling protein, Nogo receptor (NgR1), restores adult neural plasticity. Here we found that, in NgR1-deficient mice, whisker experience-driven synaptic α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) insertion in the barrel cortex, which is normally complete by 2 weeks after birth, lasts into adulthood. In vivo live imaging by two-photon microscopy revealed more AMPAR on the surface of spines in the adult barrel cortex of NgR1-deficient than on those of wild-type (WT) mice. Furthermore, we observed that whisker stimulation produced new spines in the adult barrel cortex of mutant but not WT mice, and that the newly synthesized spines contained surface AMPAR. These results suggest that Nogo signaling limits plasticity by restricting synaptic AMPAR delivery in coordination with anatomical plasticity.