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Exp Neurol. 2009 Aug;218(2):257-67. doi: 10.1016/j.expneurol.2009.03.024. Epub 2009 Mar 31.

Mitochondrial transport and docking in axons.

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Synaptic Function Section, The Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, USA.


Proper transport and distribution of mitochondria in axons and at synapses are critical for the normal physiology of neurons. Mitochondria in axons display distinct motility patterns and undergo saltatory and bidirectional movement, where mitochondria frequently stop, start moving again, and change direction. While approximately one-third of axonal mitochondria are mobile in mature neurons, a large proportion remains stationary. Their net movement is significantly influenced by recruitment to stationary or motile states. In response to the diverse physiological states of axons and synapses, the mitochondrial balance between motile and stationary phases is a possible target of regulation by intracellular signals and synaptic activity. Efficient control of mitochondrial retention (docking) at particular stations, where energy production and calcium homeostasis capacity are highly demanded, is likely essential for neuronal development and function. In this review, we introduce the molecular and cellular mechanisms underlying the complex mobility patterns of axonal mitochondria and discuss how motor adaptor complexes and docking machinery contribute to mitochondrial transport and distribution in axons and at synapses. In addition, we briefly discuss the physiological evidence how axonal mitochondrial mobility impacts synaptic function.

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