Mechanisms of protein kinase C-induced sustained activation of extracellular signal-regulated kinase in the hippocampus

被引：1
|
作者：
Kamboj, Kautuk [1 ]
Jana, Subhajit [1 ]
Sharma, Shiv K. [1 ]
机构：
[1] Natl Brain Res Ctr, Manesar 122052, Haryana, India
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2019年 / 520卷 / 02期
关键词：
Protein kinase C; Extracellular signal-regulated kinase; Long-term potentiation; Synaptic plasticity; Memory; SYNAPTIC PLASTICITY; TERM FACILITATION; MEMORY; CASCADE; INHIBITION; EXPRESSION; RAPAMYCIN; AMYGDALA; PKC; PHOSPHORYLATION;
D O I：
10.1016/j.bbrc.2019.10.046
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Protein Kinase C (PKC) and extracellular signal-regulated kinase (ERK) regulate synaptic plasticity and memory. PKC activation enhances long-term potentiation (LTP) in the hippocampal slices. In addition, activation of PKC by phorbol 12,13-diacetate (PDA) induces ERK activation. However, the mechanisms involved in PDA-induced activation of ERK are not well understood. Using hippocampal slices, we report that PDA induces a sustained activation of ERK. PDA-induced sustained ERK activation critically requires protein synthesis as well as transcription, the cellular processes that play crucial roles in long-lasting LTP and memory. In addition, the mammalian target of rapamycin activity is required for PDA-induced sustained ERK activation. Further, we show that growth factor signalling plays a critical role in PDA-induced sustained ERK activation. These results suggest that sustained ERK activation may have an important role in LTP. (C) 2019 Elsevier Inc. All rights reserved.
引用
收藏
页码：453 / 458
页数：6
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