Topic: mitochondrial trafficking

Mitochondrial trafficking is essential for neuronal development as well as for maintenance of functional mitochondrial pools at synaptic terminals. Nevertheless, the relevance of this process for mature neurons and the mechanisms governing the inherent motility of mitochondria across neuronal compartments remains unknown. By imaging mitochondrial transport in developing Purkinje neurons (PN) in situ, we observed progressive the formation of stable pools in the distal regions of dendrites, while larger dendritic calibers and axonal shaft kept a considerable extent of organelle motility up and b

Due to their large scale and uniquely branched architecture, neurons critically rely on active transport of mitochondria in order to match energy production and calcium buffering to local demand. Consequently, defective mitochondrial trafficking is implicated in various neurological and neurodegenerative diseases. A key signal regulating mitochondrial transport is intracellular calcium. Elevated Ca2+ levels have been demonstrated to inhibit mitochondrial transport in many cell types, including neurons. However, it is currently unclear to what extent calcium-signaling regulates axonal mitochond