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Rem2 稳定视觉回路的内在兴奋性和自发性放电。

Rem2 stabilizes intrinsic excitability and spontaneous firing in visual circuits.

机构信息

Department of Biology, Brandeis University, Waltham, United States.

Volen Center for Complex Systems, Brandeis University, Waltham, United States.

出版信息

Elife. 2018 May 29;7:e33092. doi: 10.7554/eLife.33092.

DOI:10.7554/eLife.33092
PMID:29809135
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6010341/
Abstract

Sensory experience plays an important role in shaping neural circuitry by affecting the synaptic connectivity and intrinsic properties of individual neurons. Identifying the molecular players responsible for converting external stimuli into altered neuronal output remains a crucial step in understanding experience-dependent plasticity and circuit function. Here, we investigate the role of the activity-regulated, non-canonical Ras-like GTPase Rem2 in visual circuit plasticity. We demonstrate that mice fail to exhibit normal ocular dominance plasticity during the critical period. At the cellular level, our data establish a cell-autonomous role for Rem2 in regulating intrinsic excitability of layer 2/3 pyramidal neurons, prior to changes in synaptic function. Consistent with these findings, both in vitro and in vivo recordings reveal increased spontaneous firing rates in the absence of Rem2. Taken together, our data demonstrate that Rem2 is a key molecule that regulates neuronal excitability and circuit function in the context of changing sensory experience.

摘要

感觉体验通过影响单个神经元的突触连接和内在特性,在塑造神经回路方面发挥着重要作用。确定将外部刺激转化为改变神经元输出的分子参与者,仍然是理解经验依赖性可塑性和回路功能的关键步骤。在这里,我们研究了活性调节的非典型 Ras 样 GTPase Rem2 在视觉回路可塑性中的作用。我们证明, 在关键期内, 小鼠无法表现出正常的眼优势可塑性。在细胞水平上,我们的数据确立了 Rem2 在调节层 2/3 锥体神经元内在兴奋性方面的细胞自主性作用,而突触功能的变化之前。与这些发现一致,无论是在体外还是在体内记录,都揭示了在没有 Rem2 的情况下自发放电率的增加。总之,我们的数据表明,Rem2 是一种关键分子,可调节神经元兴奋性和回路功能,以适应不断变化的感觉体验。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/e903b2eb72b8/elife-33092-fig10.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/bab7660599f6/elife-33092-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/8a2630d29988/elife-33092-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/863fa71fd5ef/elife-33092-fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/c1ff5f1f8712/elife-33092-fig8-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/dc7c43771b08/elife-33092-fig9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/e903b2eb72b8/elife-33092-fig10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/ed598b93371e/elife-33092-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/a5d1e7774ec8/elife-33092-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/10f229b75bdf/elife-33092-fig2-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/0179440b2375/elife-33092-fig2-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/ccd7e255d3ef/elife-33092-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/1063a8e09914/elife-33092-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/398a20fed96e/elife-33092-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/bab7660599f6/elife-33092-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/8a2630d29988/elife-33092-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/863fa71fd5ef/elife-33092-fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/c1ff5f1f8712/elife-33092-fig8-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/dc7c43771b08/elife-33092-fig9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/844c/6010341/e903b2eb72b8/elife-33092-fig10.jpg

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