An examination of the effects of mitochondrial transport disruption in cortical neurons and astrocytes

Recent studies have revealed that mitochondria are mobile structures within neurons and are transported by molecular motors associated with the cytoskeleton. The significance of mitochondrial motility is unknown although it may be connected to intracellular ATP distribution and/or calcium sequestration. Therefore, disrupted mitochondrial translocation may compromise these functions and contribute to neuronal injury. In this study we inhibited mitochondrial trafficking by disrupting the dynactin complex and observed the effects on mitochondrial dynamics. In comparison to control cells, mitochondria were smaller and were largely absent from peripheral regions of astrocytes and the amount of mitochondrial movement exhibited by transport-disrupted cells was severely diminished. Calcium uptake and mitochondrial membrane potential were also significantly reduced. Cell survival after glutamate challenge was unaffected. These studies give us some insight into the importance of mitochondrial transport in neuronal health