线粒体
突触
遗传性痉挛性截瘫
神经科学
生物
细胞生物学
肌萎缩侧索硬化
表型
医学
基因
遗传学
病理
疾病
作者
Cindy V. Ly,Patrik Verstreken
标识
DOI:10.1177/1073858406287661
摘要
Synapses are packed with mitochondria, complex organelles with roles in energy metabolism, cell signaling, and calcium homeostasis. However, the precise mechanisms by which mitochondria influence neurotrans mission remain undefined. In this review, the authors discuss pharmacological and genetic analyses of synaptic mitochondrial function, focusing on their role in Ca 2+ buffering and ATP production. Additionally, they will summarize recent data that implicate synaptic mitochondria in the regulation of neurotransmitter release during intense neuronal activity and link these findings to the pathogenesis of neurodegenerative diseases that feature disrupted synaptic mitochondria, including amyotrophic lateral sclerosis and hereditary spastic paraplegia.
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