Maintenance of synaptic homeostasis is a challenging task, due to the intricate spatial organization and intense activity of synapses. Typically, synapses are located far away from the neuronal cell body, where they orchestrate neuronal signalling and communication, through neurotransmitter release. Stationary mitochondria provide energy required for synaptic vesicle cycling, and preserve ionic balance by buffering intercellular calcium at synapses. Thus, synaptic homeostasis is critically dependent on proper mitochondrial function. Indeed, defective mitochondrial metabolism is a common feature of several neurodegenerative and psychiatric disorders, including Alzheimer's disease (AD), Parkinson's disease (PD), bipolar disorders and schizophrenia among others, which are also accompanied by excessive synaptic abnormalities. Specialized and compartmentalized quality control mechanisms have evolved to restore and maintain synaptic energy metabolism. Here, we survey recent advances towards the elucidation of the pivotal role of mitochondria in neurotransmission and implicating mitophagy in the maintenance of synaptic homeostasis during ageing.

中文翻译：

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突触中线粒体的调控和作用。

由于复杂的空间组织和突触的激烈活动，维持突触稳态是一项艰巨的任务。通常，突触位于远离神经元细胞体的位置，在那里它们通过神经递质的释放来协调神经元的信号传导和通讯。固定线粒体提供了突触小泡循环所需的能量，并通过在突触处缓冲细胞间钙来保持离子平衡。因此，突触稳态主要取决于适当的线粒体功能。实际上，线粒体代谢缺陷是几种神经退行性和精神病性疾病的常见特征，包括阿尔茨海默氏病（AD），帕金森氏病（PD），双相情感障碍和精神分裂症等，还伴有过度的突触异常。专门的和分隔的质量控制机制已经发展为恢复和维持突触能量代谢。在这里，我们调查了阐明线粒体在神经传递中的关键作用以及在衰老过程中牵涉线粒体维持突触稳态的最新进展。