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Fission and Fusion of the Neuronal Endoplasmic Reticulum

机译:神经元内质网的分裂与融合

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The endoplasmic reticulum (ER) is central for protein synthesis and is the largest intracellular Ca2+ store in neurons. The neuronal ER is classically described to have a continuous lumen spanning all cellular compartments. This allows neuronal ER to integrate spatially separate events in the cell. Recent in vitro as well as in vivo findings, however, demonstrate that the neuronal ER is a structurally dynamic entity, capable of rapid fragmentation, i.e., ER fission. The ER fragments can fuse back together and reinstate ER continuity. This reversible phenomenon can be induced repeatedly within the same cell, is temperature-dependent, and compatible with cell survival. The key trigger for dendritic ER fission is N-methyl D-aspartate (NMDA) receptor stimulation in the presence of extracellular Ca2+. However, the exact molecular machinery responsible for the fission and fusion of neuronal ER remains unknown. Reversible ER fission represents a new cell biological event downstream of NMDA receptor-gated Ca2+ influx and may thus influence many aspects of neuronal function in physiology and disease. Hence, it constitutes a new field for exploration in neuroscience that will benefit greatly from recent advances in light microscopy imaging techniques allowing dynamic characterization of cellular events in vitro and in vivo.
机译:内质网(ER)是蛋白质合成的中心,并且是神经元中最大的细胞内Ca2 +存储。传统上将神经元ER描述为具有跨越所有细胞区室的连续内腔。这使神经元ER能够整合细胞中空间独立的事件。然而,最近的体外和体内发现表明,神经元ER是一种结构动态的实体,能够快速断裂,即ER裂变。 ER片段可以融合在一起,并恢复ER的连续性。这种可逆现象可以在同一细胞内反复诱发,是温度依赖性的,并且与细胞存活相容。在细胞外Ca2 +存在下,树突状ER裂变的关键触发因素是N-甲基D-天冬氨酸(NMDA)受体刺激。然而,负责神经元内质网裂变和融合的确切分子机制仍然未知。可逆的ER裂变代表NMDA受体门控的Ca2 +流入下游的新细胞生物学事件,因此可能影响生理和疾病中神经元功能的许多方面。因此,它构成了神经科学探索的新领域,它将极大地受益于光学显微镜成像技术的最新进展,该技术允许对体内和体外的细胞事件进行动态表征。

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