Molecular mechanisms controlling protein synthesis in memory reconsolidation

被引:28
|
作者
Roesler, Rafael [1 ,2 ]
机构
[1] Univ Fed Rio Grande do Sul, Inst Basic Hlth Sci, Dept Pharmacol, BR-90050170 Porto Alegre, RS, Brazil
[2] Univ Fed Rio Grande do Sul, Clin Hosp CPE HCPA, Expt Res Ctr, Canc & Neurobiol Lab, BR-90035003 Porto Alegre, RS, Brazil
关键词
Protein synthesis; Translation control; Rapamycin Mechanistic target of rapamycin; Fear memory; Memory reconsolidation; LONG-TERM-MEMORY; INHIBITORY AVOIDANCE MEMORY; LASTING SYNAPTIC PLASTICITY; TUBEROUS SCLEROSIS COMPLEX; MAMMALIAN TARGET; FEAR MEMORY; TRANSLATIONAL CONTROL; DORSAL HIPPOCAMPUS; SIGNALING PATHWAY; S6; KINASE;
D O I
10.1016/j.nlm.2017.04.015
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
It is currently well established that the synthesis of new proteins (mRNA translation) is required for longlasting synaptic plasticity and memory formation. Translation in the brain is regulated primarily at the initiation stage by general as well as by gene-specific mechanisms. Stored memories can become sensitive to interference upon reactivation, through a process termed reconsolidation, which depends on protein synthesis. Here, I examine the role of translation control mechanisms, focusing particularly on the mechanistic target of rapamycin complex 1 (mTORC1), in reconsolidation. (C) 2017 Elsevier Inc. All rights reserved.
引用
收藏
页码:30 / 40
页数:11
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