Axoplasmic transport

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File:Cytoplasmic dynein.PNG
Dynein, a motor protein responsible for retrograde axonal transport, carries vesicles and other cellular products toward the cell bodies of neurons. Its light chains bind the cargo, and its globular head regions bind the microtubule, inching along it.

Axoplasmic transport, also called axonal transport, is responsible for movement of mitochondria, lipids, synaptic vesicles, proteins, and other cell parts to and from a neuron's cell body through the cytoplasm of its axon (the axoplasm). Axons, which can be 1,000 or 10,000 times the length of the cell body, or soma, contain no ribosomes or means of producing proteins, and so rely on axoplasmic transport for all their protein needs.[1][2] Axonal transport is also responsible for moving molecules destined for degradation from the axon to lysosomes to be broken down.[3] Movement toward the cell body is called retrograde transport and movement toward the synapse is called anterograde transport.[1]


The vast majority of axonal proteins are synthesized in the neuronal cell body and transported along axons. Axonal transport occurs throughout the life of a neuron and is essential to its growth and survival. Microtubules lie along the axis of the axon and provide the main cytoskeletal "tracks" for transport. The motor proteins kinesin and dynein are mechanochemical enzymes that move cargoes anterogradely (towards the axon tip) and retrogradely (towards the cell body) respectively. The motor proteins bind and carries organelles, mitochondria, cytoskeletal polymers, neurotransmitters etc.[1][4]

While vesicular cargoes in fast transport were readily visualized and many kinesins and dyneins moving them were characterized, general mechanisms of slow axonal transport had been controversial for decades, as the movement was difficult to directly visualize. [5] In particular, it was unclear how the slow movement could be generated using the "fast" moving motor proteins in axons. This issue has been resolved by recent studies that were able to directly visualize the slow transport of cytoskeletal polymers like neurofilaments, microtubules as well as other slow cytosolic cargoes in living neurons. These studies showed that surprizingly, the movement of individual slow cargoes is rapid, similar to that of fast cargoes, but unlike fast cargoes, slow cargoes pause frequently during transit and this makes the overall movement of the slow component much slower. An analogy is the difference in transport rates between a local and an express subway train. Though both trains move at similar velocities between stations, the local is much slower overall than an an express due to frequent pausing at every station, as opposed to an express train that makes only a few stops. This is now known as the "Stop and Go" model of slow axonal transport [6][7]

Anterograde transport

Axonal transport can be divided into anterograde and retrograde categories and further divided into fast and slow subtypes. The rapid movement of individual cargoes of both fast and slow components indicate that all anterograde transport is mediated by kinesins. Indeed, several kinesins have been implicated in slow transport [5], however, the mechanism generating the "pauses" in the transit of slow component cargoes is still unknown.

There are two classes of slow anterograde transport: slow component a (SCa) that carries mainly microtubules and neurofilaments at 0.1-1 millimeter per day, and slow component b (SCb) that carries over 200 diverse proteins and actin at a rate of up to six millimeters a day.[5]

Retrograde transport

Retrograde transport, which is mediated by dynein, sends chemical messages, and endocytosis products headed to endolysosomes from the axon back to the cell.[3] Fast retrograde transport can cover 100-200 millimeters per day.[3]

Consequences of interruption

Since the axon depends on axoplasmic transport for vital proteins and materials, injury such as diffuse axonal injury that interrupts the transport will cause the distal axon to degenerate in a process called Wallerian degeneration. Dysfunctional axonal transport is also linked to neurdegenerative disease such as Alzheimer's.[5]

Cancer drugs that interfere with cancerous growth by altering microtubules (which are necessary for cell division) damage nerves because the microtubules are necessary for axonal transport.[1]


  1. 1.0 1.1 1.2 1.3 Cowie R.J. and Stanton G.B. "Axoplasmic Transport and Neuronal Responses to Injury." Howard University College of Medicine. Retrieved on January 25, 2007.
  2. Sabry J., O’Connor T. P., and Kirschner M. W. 1995. Axonal Transport of Tubulin in Ti1 Pioneer Neurons in Situ. Neuron. 14(6): 1247-1256. PMID 7541635. Retrieved on January 25, 2007.
  3. 3.0 3.1 3.2 Oztas E. 2003. Neuronal Tracing. Neuroanatomy. 2: 2-5. Retrieved on January 25, 2007.
  4. Karp G. 2005. Cell and Molecular Biology: Concepts and Experiments, Fourth ed, p. 344. John Wiley and Sons, Hoboken, NJ. ISBN 0471465801
  5. 5.0 5.1 5.2 5.3 Roy S, et al. 2005. Axonal transport defects: a common theme in neurodegenerative Acta Neuropathol 109: 5-13. PMID 15645263.
  6. Brown 2003. "Axonal transport of membranous and nonmembranous cargoes: a unified perspective", J Cell Biol. 2003 Mar 17;160(6):817-21
  7. Roy S et al., 2007. "Rapid and intermittent cotransport of slow component-b proteins". J Neurosci. 2007 Mar 21;27(12):3131-8