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γ-氨基丁酸受体的转录后基因调控以控制神经元抑制作用

Posttranscriptional Gene Regulation of the GABA Receptor to Control Neuronal Inhibition.

作者信息

Schieweck Rico, Kiebler Michael A

机构信息

Department of Cell Biology and Anatomy, Medical Faculty, Biomedical Center (BMC), Ludwig-Maximilians-University of Munich, Munich, Germany.

出版信息

Front Mol Neurosci. 2019 Jun 25;12:152. doi: 10.3389/fnmol.2019.00152. eCollection 2019.

DOI:10.3389/fnmol.2019.00152
PMID:31316346
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6611381/
Abstract

Behavior and higher cognition rely on the transfer of information between neurons through specialized contact sites termed synapses. Plasticity of neuronal circuits, a prerequisite to respond to environmental changes, is intrinsically coupled with the nerve cell's ability to form, structurally modulate or remove synapses. Consequently, the synaptic proteome undergoes dynamic alteration on demand in a spatiotemporally restricted manner. Therefore, proper protein localization at synapses is essential for synaptic function. This process is regulated by: (i) protein transport and recruitment; (ii) local protein synthesis; and (iii) synaptic protein degradation. These processes shape the transmission efficiency of excitatory synapses. Whether and how these processes influence synaptic inhibition is, however, widely unknown. Here, we summarize findings on fundamental regulatory processes that can be extrapolated to inhibitory synapses. In particular, we focus on known aspects of posttranscriptional regulation and protein dynamics of the GABA receptor (GABAR). Finally, we propose that local (co)-translational control mechanism might control transmission of inhibitory synapses.

摘要

行为和高级认知依赖于神经元之间通过称为突触的特殊接触位点进行信息传递。神经回路的可塑性是对环境变化做出反应的先决条件,它与神经细胞形成、结构调节或消除突触的能力内在相关。因此,突触蛋白质组会根据需求以时空受限的方式进行动态改变。因此,突触处蛋白质的正确定位对于突触功能至关重要。这一过程受以下因素调节:(i)蛋白质运输和募集;(ii)局部蛋白质合成;以及(iii)突触蛋白质降解。这些过程塑造了兴奋性突触的传递效率。然而,这些过程是否以及如何影响突触抑制,目前仍知之甚少。在这里,我们总结了可外推至抑制性突触的基本调节过程的研究结果。特别是,我们关注γ-氨基丁酸受体(GABAR)转录后调控和蛋白质动态的已知方面。最后,我们提出局部(共)翻译控制机制可能控制抑制性突触的传递。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c79d/6611381/17c8b367f8c9/fnmol-12-00152-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c79d/6611381/503ebfc031d2/fnmol-12-00152-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c79d/6611381/756067acff20/fnmol-12-00152-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c79d/6611381/17c8b367f8c9/fnmol-12-00152-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c79d/6611381/503ebfc031d2/fnmol-12-00152-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c79d/6611381/756067acff20/fnmol-12-00152-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c79d/6611381/17c8b367f8c9/fnmol-12-00152-g0003.jpg

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