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Abstract
In order to satisfy the metabolic and ion homeostasis demands of neurons, mitochondria must be transported to appropriate locations within cells. Although it is well established that much of this trafficking occurs on microtubules and, to a lesser extent, actin, the mechanisms by which the trafficking of mitochondria is controlled are poorly understood. A recent study by Chada and Hollenbeck shows that nerve growth factor halts the movement of mitochondria in axons by means of a mechanism that depends on activation of phosphatidylinositol 3-kinase. These studies provide important new insights into the mechanisms that regulate mitochondrial movement and control mitochondrial docking. These insights are critical to the understanding of the factors that control the distribution, location, and function of mitochondria in both healthy and injured neurons.
