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体树突解耦作为皮质长期成熟的一种新机制。

Somato-dendritic decoupling as a novel mechanism for protracted cortical maturation.

作者信息

Chomiak Taylor, Hung Johanna, Nguyen Minh Dang, Hu Bin

机构信息

Division of Translational Neuroscience, Department of Clinical Neurosciences, Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, T2N 4N1, Canada.

出版信息

BMC Biol. 2016 Jun 21;14:48. doi: 10.1186/s12915-016-0270-5.

DOI:10.1186/s12915-016-0270-5
PMID:27328836
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4916537/
Abstract

BACKGROUND

Both human and animal data indicate that disruption of the endogenously slow maturation of temporal association cortical (TeA) networks is associated with abnormal higher order cognitive development. However, the neuronal mechanisms underlying the endogenous maturation delay of the TeA are poorly understood.

RESULTS

Here we report a novel form of developmental plasticity that is present in the TeA. It was found that deep layer TeA neurons, but not hippocampal or primary visual neurons, exist in a protracted 'embryonic-like' state through a mechanism involving reduced somato-dendritic communication and a non-excitable somatic membrane. This mechanism of neural inactivity is present in intact tissue and shows a remarkable transition into an active somato-dendritically coupled state. The quantity of decoupled cells diminishes in a protracted and age-dependent manner, continuing into adolescence.

CONCLUSIONS

Based on our data, we propose a model of neural plasticity through which protracted compartmentalization and decoupling in somato-dendritic signalling plays a key role in controlling how excitable neurons are incorporated into recurrent cortical networks independent of neurogenesis.

摘要

背景

人类和动物数据均表明,颞叶联合皮质(TeA)网络内源性缓慢成熟的破坏与异常的高阶认知发展相关。然而,TeA内源性成熟延迟的神经元机制仍知之甚少。

结果

在此,我们报告了一种存在于TeA中的新型发育可塑性形式。研究发现,深层TeA神经元而非海马或初级视觉神经元,通过一种涉及体细胞 - 树突通信减少和非兴奋性体细胞细胞膜的机制,处于一种持续的“胚胎样”状态。这种神经无活动状态存在于完整组织中,并显示出向活跃的体细胞 - 树突耦合状态的显著转变。解耦细胞的数量以持续且依赖年龄的方式减少,一直持续到青春期。

结论

基于我们的数据,我们提出了一种神经可塑性模型,通过该模型,体细胞 - 树突信号传导中的持续分隔和解耦在控制兴奋性神经元如何独立于神经发生而融入递归皮质网络中起着关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0384/4916537/f34288ea8b3d/12915_2016_270_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0384/4916537/7583718c4e7a/12915_2016_270_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0384/4916537/fc27bf2eb150/12915_2016_270_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0384/4916537/2bc445efd707/12915_2016_270_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0384/4916537/abc43a742ceb/12915_2016_270_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0384/4916537/f34288ea8b3d/12915_2016_270_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0384/4916537/7583718c4e7a/12915_2016_270_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0384/4916537/fc27bf2eb150/12915_2016_270_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0384/4916537/2bc445efd707/12915_2016_270_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0384/4916537/abc43a742ceb/12915_2016_270_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0384/4916537/f34288ea8b3d/12915_2016_270_Fig5_HTML.jpg

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