兴奋毒性
谷氨酸受体
神经科学
致电离效应
线粒体通透性转换孔
NMDA受体
生物
谷氨酸的
兴奋性突触后电位
去极化
细胞外
线粒体
神经递质
红藻氨酸
化学
细胞生物学
中枢神经系统
抑制性突触后电位
受体
程序性细胞死亡
生物物理学
生物化学
细胞凋亡
作者
Sam M. Greenwood,Christopher N. Connolly
标识
DOI:10.1016/j.neuropharm.2007.10.003
摘要
Glutamate is the predominant excitatory neurotransmitter in the mammalian central nervous system (CNS) and is normally stored intracellularly. However, in instances of CNS injury or disease, increased concentrations of extracellular glutamate can result in the over-activation of ionotropic glutamate receptors and trigger neuronal cell death (termed excitotoxicity). Two early hallmarks of such neuronal toxicity are mitochondrial dysfunction (depolarisation, decreased ATP synthesis, structural collapse and potential opening of the permeability transition pore) and the formation of focal swellings (also termed varicosities/beads) along the length of the dendrites. In this review, we summarise current knowledge of the mechanisms that underlie these early excitotoxic events as well as the mechanisms that facilitate dendritic recovery following termination of the excitotoxic insult.
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