Department of Neuropharmacology, Interdisciplinary Graduate School of Medicine, University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi 409-3898, Japan.
Department of Neuropharmacology, Interdisciplinary Graduate School of Medicine, University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi 409-3898, Japan.
Neurochem Int. 2018 Oct;119:107-114. doi: 10.1016/j.neuint.2018.01.007. Epub 2018 Feb 2.
The brain consists of neurons and much higher number of glial cells. They communicate each other, by which they control brain functions. The brain is highly vulnerable to several insults such as ischemia, but has a self-protective and self-repairing mechanisms against these. Ischemic tolerance or preconditioning is an endogenous neuroprotective phenomenon, where a mild non-lethal ischemic episode can induce resistance to a subsequent severe ischemic injury in the brain. Because of its neuroprotective effects against cerebral ischemia or stroke, ischemic tolerance has been widely studied. However, almost all studies have been performed from the viewpoint of neurons. Glial cells are structurally in close association with synapses. Recent studies have uncovered the active roles of astrocytes in modulating synaptic connectivity, such as synapse formation, elimination and maturation, during development or pathology. However, glia-mediated ischemic tolerance and/or neuronal repairing have received only limited attention. We and others have demonstrated that glial cells, especially astrocytes, play a pivotal role in regulation of induction of ischemic tolerance as well as repairing/remodeling of neuronal networks by phagocytosis. Here, we review our current understanding of (1) glial-mediated ischemic tolerance and (2) glia-mediated repairing/remodeling of the penumbra neuronal networks, and highlight their mechanisms as well as their potential benefits, problems, and therapeutic application.
大脑由神经元和数量更多的神经胶质细胞组成。它们通过相互交流来控制大脑功能。大脑容易受到多种损伤的影响，如缺血，但它具有自我保护和自我修复机制来对抗这些损伤。缺血耐受或预处理是一种内源性的神经保护现象，其中轻度的非致死性缺血发作可以诱导大脑对随后的严重缺血损伤产生抗性。由于其对脑缺血或中风的神经保护作用，缺血耐受已被广泛研究。然而，几乎所有的研究都是从神经元的角度进行的。神经胶质细胞在结构上与突触密切相关。最近的研究揭示了星形胶质细胞在调节突触连接中的积极作用，例如在发育或病理过程中突触的形成、消除和成熟。然而，神经胶质细胞介导的缺血耐受和/或神经元修复仅受到有限的关注。我们和其他人已经证明，神经胶质细胞，特别是星形胶质细胞，在调节缺血耐受的诱导以及吞噬作用介导的神经元网络的修复/重塑中发挥关键作用。在这里，我们回顾了我们对（1）神经胶质细胞介导的缺血耐受和（2）神经胶质细胞介导的半影区神经元网络修复/重塑的理解，并强调了它们的机制以及它们的潜在益处、问题和治疗应用。
