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通过A激酶锚定蛋白(AKAP)信号复合物对突触可塑性进行调控。

Orchestration of synaptic plasticity through AKAP signaling complexes.

作者信息

Bauman Andrea L, Goehring April S, Scott John D

机构信息

Howard Hughes Medical Institute, Vollum Institute, Oregon Health & Science University, Portland, OR 97239, USA.

出版信息

Neuropharmacology. 2004 Mar;46(3):299-310. doi: 10.1016/j.neuropharm.2003.09.016.

DOI:10.1016/j.neuropharm.2003.09.016
PMID:14975685
Abstract

Significant progress has been made toward understanding the mechanisms by which organisms learn from experiences and how those experiences are translated into memories. Advances in molecular, electrophysiological and genetic technologies have permitted great strides in identifying biochemical and structural changes that occur at synapses during processes that are thought to underlie learning and memory. Cellular events that generate the second messenger cyclic AMP (cAMP) and activate protein kinase A (PKA) have been linked to synaptic plasticity and long-term memory. In this review we will focus on the role of PKA in synaptic plasticity and discuss how the compartmentalization of PKA through its association with A-Kinase Anchoring Proteins (AKAPs) affect PKA function in this process.

摘要

在理解生物体从经验中学习的机制以及这些经验如何转化为记忆方面已经取得了重大进展。分子、电生理和基因技术的进步使得在识别被认为是学习和记忆基础的过程中突触发生的生化和结构变化方面取得了巨大进展。产生第二信使环磷酸腺苷(cAMP)并激活蛋白激酶A(PKA)的细胞事件与突触可塑性和长期记忆有关。在这篇综述中,我们将重点关注PKA在突触可塑性中的作用,并讨论PKA通过与A激酶锚定蛋白(AKAPs)结合而进行的区室化如何影响该过程中PKA的功能。

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Orchestration of synaptic plasticity through AKAP signaling complexes.通过A激酶锚定蛋白(AKAP)信号复合物对突触可塑性进行调控。
Neuropharmacology. 2004 Mar;46(3):299-310. doi: 10.1016/j.neuropharm.2003.09.016.
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