Mitochondrial support and local translation of mitochondrial proteins in synaptic plasticity and function.

Abstract

Complex neural and brain functions are executed through structural and functional alterations of synapses and neurons. Neuronal compartmentalization requires neurons to allocate mitochondria and proteins in a spatiotemporal manner to allow their plasticity, function and homeostasis. Importantly, mitochondria are known to interact with and modulate synaptic activities through their ATP supply, calcium buffering and signaling abilities. Over the years, mitochondrial support and local translation (including mitochondrial proteins) at neuronal sub-compartments and their synaptic specializations have been considered critical for maintaining synaptic plasticity and function. Recently, evidence has shown that late endosomes can serve as sites for local translation of mRNAs crucial for mitochondrial integrity and mitochondrial compartments can fuel plasticity-induced local translation. Indeed, failed mitochondrial homeostasis and subsequent synaptic dysfunction are often intricately linked in the malfunction of the central nervous system in synaptic aging and diseases. In this review, I will discuss the critical role of local translation (including mitochondrial proteins) in dendrites, axons and synapses on neuronal/synaptic plasticity and function.