Glia: guardians, gluttons, or guides for the maintenance of neuronal connectivity?
Glia: guardians, gluttons, or guides for the maintenance of neuronal connectivity?
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DOI：
10.1111/nyas.12711
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发表时间：
2015-09
影响因子：
5.2
通讯作者：
Garden GA
中科院分区：
文献类型：
--
作者：
Jebelli J;Su W;Hopkins S;Pocock J;Garden GA
神经元-胶质细胞相互作用的一个新兴方面是胶质细胞与突触的连接。现在越来越多的研究表明，这种关系比以前认识到的要亲密得多。此外，目前表明神经退行性疾病病因学中突触缺失的证据是压倒性的，但神经胶质细胞在突触变性过程中的作用直到最近才被认真考虑。神经胶质细胞的每个主要类别，包括星形胶质细胞、少突胶质细胞和小胶质细胞，在维持突触功能和兴奋性方面发挥着至关重要的多方面作用。因此，来自疾病相关错误折叠蛋白的衰老和/或神经元应激可能涉及由邻近神经胶质介导的多个非细胞自主突触支持系统的破坏。此外，损伤、缺血或神经变性诱导的神经胶质细胞激活被认为会极大地改变神经胶质细胞对神经元突触的行为，这表明神经炎症可能导致主要由神经胶质功能改变介导的突触丧失。本综述讨论了最近的证据，强调了神经胶质细胞在神经元突触和维持神经元连接中的新作用，主要关注它们对神经退行性疾病研究的影响。
An emerging aspect of neuronal–glial interactions is the connection glial cells have to synapses. Mounting research now suggests a far more intimate relationship than previously recognized. Moreover, the current evidence implicating synapse loss in neurodegenerative disease etiology is overwhelming, but the role of glia in the process of synaptic degeneration has only recently been considered in earnest. Each main class of glial cell, including astrocytes, oligodendrocytes, and microglia, performs crucial and multifaceted roles in the maintenance of synaptic function and excitability. As such, aging and/or neuronal stress from disease-related misfolded proteins may involve disruption of multiple non-cell-autonomous synaptic support systems that are mediated by neighboring glia. In addition, glial cell activation induced by injury, ischemia, or neurodegeneration is thought to greatly alter the behavior of glial cells toward neuronal synapses, suggesting that neuroinflammation potentially contributes to synapse loss primarily mediated by altered glial functions. The present review discusses recent evidence highlighting novel roles for glial cells at neuronal synapses and in the maintenance of neuronal connectivity, focusing primarily on their implications for neurodegenerative disease research.