Synaptic signaling by lipids in the life and death of neurons
Synaptic signaling by lipids in the life and death of neurons
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DOI：
10.1385/mn:31:1-3:219
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发表时间：
2005-01-01
影响因子：
5.1
通讯作者：
Bazan, NG
中科院分区：
文献类型：
--
作者：
Bazan, NG
突触活动通过磷脂酶介导的从膜上切割特定磷脂库来促进脂质信使的调节形成。多种效应物触发脂质信使的形成，包括神经递质、膜去极化、离子通道、细胞因子和神经营养因子。脂质信使反过来调节其他信号级联并与之相互作用，从而促进发育、分化、功能（例如，长时程增强（LTP）和记忆），保护和修复神经系统细胞。这些与其他信号级联的关系仍有待进一步研究。氧化应激破坏脂质信号传导，增强脂质过氧化，并引发和传播神经变性。越来越多的证据表明，脂质信使参与神经元、星形胶质细胞、少突胶质细胞、小胶质细胞、微血管细胞和其他细胞之间的广泛相互作用。本文提供了一个例子，如何通过脂质信号调节神经元存活必不可少的关键事件，并回顾了最近发现的一种新的内源性神经保护信号通路，涉及二十二碳六烯酸衍生的介质。
Synaptic activity promotes the regulated formation of lipid messengers through phospholipase-mediated cleavage of specific phospholipid reservoirs from membranes. Multiple effectors trigger the formation of lipid messengers, including neurotransmitters, membrane depolarization, ion channels, cytokines, and neurotrophic factors. Lipid messengers in turn modulate and interact with other signaling cascades, contributing to the development, differentiation, function (e.g., long-term potentiation [LTP] and memory), protection, and repair of cells in the nervous system. These relationships with other signaling cascades remain largely to be investigated. Oxidative stress disrupts lipid signaling, enhances lipid peroxidation, and initiates and propagates neurodegeneration. There is growing evidence that lipid messengers participate in the extensive interactions among neurons, astrocytes, oligodendrocytes, microglia, cells of the microvasculature, and other cells. This article provides an example of how signaling by lipids regulates critical events essential for neuronal survival and reviews the recent identification of a novel endogenous neuroprotective signaling pathway involving a docosahexaenoic acid-derived mediator.