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Effects of neuroinflammation on glia-glia gap junctional intercellular communication: a perspective.

机译:神经炎症对神经胶质-神经胶质间隙连接细胞间通讯的影响:一个观点。

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摘要

Gap junctions serve as intercellular conduits that allow for the direct transfer of small molecular weight molecules (up to 1 kDa) including ions involved in cellular excitability, metabolic precursors, and second messengers. The observation of extensive intercellular coupling and large numbers of gap junctions in the central nervous system (CNS) suggests a syncytium-like organization of glial compartments. Inflammation is a hallmark of various CNS diseases such as bacterial and viral infections, multiple sclerosis, Alzheimer's disease, and cerebral ischemia. A general consequence of brain inflammation is reactive gliosis typified by astrocyte hypertrophy and proliferation of astrocytes and microglia. Changes in gap junction intercellular communication as reflected by alterations in dye coupling and connexin expression have been associated with numerous CNS inflammatory diseases, which may have dramatic implications on the survival of neuronal and glial populations in the context of neuroinflammation. A review of the effects of inflammatory products on glia-glia gap junctional communication and glial glutamate release is presented. In addition, the hypothesis of a "syncytial switch" based upon differential regulation of gap junction expression in astrocytes and microglia during normal CNS homeostasis and neuroinflammation is proposed.
机译:间隙连接用作细胞间导管,可直接转移小分子量分子(最大1 kDa),包括涉及细胞兴奋性的离子,代谢前体和第二信使。在中枢神经系统(CNS)中广泛的细胞间偶联和大量的间隙连接的观察表明胶质区室的合胞体状组织。炎症是各种中枢神经系统疾病的标志,例如细菌和病毒感染,多发性硬化症,阿尔茨海默氏病和脑缺血。脑部炎症的一般后果是以星形胶质细胞肥大,星形胶质细胞和小胶质细胞增生为代表的反应性神经胶质增生。染料偶联和连接蛋白表达的改变所反映的间隙连接细胞间通讯的变化已与许多中枢神经系统炎性疾病有关,这可能对神经发炎情况下神经元和神经胶质细胞群体的存活产生重大影响。综述了炎症产物对神经胶质-神经胶质间隙连接通讯和神经胶质谷氨酸释放的影响。此外,提出了基于正常中枢神经系统稳态和神经炎症过程中星形胶质细胞和小胶质细胞间隙连接表达差异调节的“合胞开关”的假说。

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