Synapse reorganization-a new partnership revealed.
Synapse reorganization-a new partnership revealed.
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Synapse 重组——新的合作伙伴关系揭晓。
DOI：
10.1002/embj.201488619
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Hayashi Y.
中科院分区：
文献类型：
--
作者：
Saneyoshi T;Hayashi Y.
突触功能的改变需要突触成分的定性和定量重组。Ca2+在这一过程中起核心作用，但其机制尚未完全阐明。zhang等报道了Ca2+/calmodulin （CaM）调节突触后支架稳定性的新机制。Ca2+/CaM与PSD‐95相互作用，PSD‐95是突触后密度（PSD）的核心蛋白，支持突触信号传导和结构成分。Ca2+/CaM干扰PSD‐95的棕榈酰化，导致PSD‐95与突触后膜分离。这一过程可以解释突触抑制过程中观察到的表面谷氨酸受体的减少和神经元活动延长后突触反应的稳态调节。
Changes in synaptic function require both qualitative and quantitative reorganization of the synaptic components. Ca2+plays a central role in this process, but the mechanism has not been fully elucidated. Zhanget alreport a novel mechanism whereby Ca2+/calmodulin (CaM) regulates the stability of the postsynaptic scaffold. Ca2+/CaM interacts with PSD‐95, a core protein in the postsynaptic density (PSD) that supports synaptic signaling and structural components. Ca2+/CaM interferes with the palmitoylation of PSD‐95, resulting in the dissociation of PSD‐95 from the postsynaptic membrane. This process may explain the reduction of surface glutamate receptor observed during synaptic depression and homeostatic regulation of the synaptic response after prolonged neuronal activity.