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突触后的自噬始于Rab11,且并不随着树突棘修剪而结束。

Autophagy at the postsynapse begins with Rab11 and does not end with dendritic spine pruning.

作者信息

Janusz-Kaminska Aleksandra, Jaworski Jacek

机构信息

Department of Cell Biology, Emory University School of Medicine, Atlanta, GA, USA.

Laboratory of Molecular and Cellular Neurobiology, International Institute of Molecular and Cell Biology in Warsaw, Warsaw, Poland.

出版信息

Autophagy Rep. 2024 May 1;3(1):2346064. doi: 10.1080/27694127.2024.2346064. eCollection 2024.

Abstract

Neurons are highly differentiated and compartmentalized cells that conduct cellular processes in a spatiotemporally regulated manner. Autophagy in neurons occurs locally under stimulation and contributes to synaptic plasticity. Little is known about the initial steps leading to autophagy upon neuronal stimulation and the role of autophagic compartments at the postsynaptic part of the synapse. Here, we summarize our recent manuscript on Rab11 role in autophagy initiation in the dendritic spines. We showed that Rab11 maintains in the dendritic spines Atg9A and is necessary for LC3+ vesicles to emerge at the postsynapse. We hypothesize that autophagosomes arise due to an interplay between NMDA receptor stimulation and local mTOR kinase activity. We suggest that autophagosomes are not, in fact, responsible for dendritic spine pruning.

摘要

神经元是高度分化且具有区室化的细胞,它们以时空调节的方式进行细胞活动。神经元中的自噬在刺激下局部发生,并有助于突触可塑性。关于神经元刺激后导致自噬的初始步骤以及自噬区室在突触后突触部分的作用,我们知之甚少。在这里,我们总结了我们最近关于Rab11在树突棘自噬起始中作用的手稿。我们表明,Rab11在树突棘中维持Atg9A,并且是LC3+囊泡在突触后出现所必需的。我们假设自噬体的产生是由于NMDA受体刺激和局部mTOR激酶活性之间的相互作用。我们认为,事实上自噬体并不负责树突棘的修剪。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/001b/11864627/0731ffb443d0/KAUO_A_2346064_F0001_OC.jpg

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