My watch list  

Axoplasmic transport


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. Motor proteins bind and transport several different cargoes including organelles such as mitochondria, cytoskeletal polymers, and vesicles containing neurotransmitter.[1][4]

Axonal transport can be divided into anterograde and retrograde categories and further divided into fast and slow subtypes.

Fast and slow transport

Vesicular cargoes move relatively fast (50-400 mm/day) whereas transport of proteins takes much longer (moving at less than 8 mm/day). Fast axonal transport has been understood for decades but the mechanism of slow axonal transport has only recently been discovered as experimental techniques have improved.[5] Fluorescent labelling techniques have enabled direct visualization of transport in living neurons. Recent studies have revealed that the movement of individual "slow" cargoes is actually rapid but unlike fast cargoes, they pause frequently, making the overall transit rate much slower. The mechanism is known as the "Stop and Go" model of slow axonal transport.[6][7] An analogy is the difference in transport rates between local and express subway trains. Though both types of train travel at similar velocities between stations, the local train takes much longer to reach the end of the line because it stops at every station whereas the express makes only a few stops on the way.

Anterograde (orthograde) transport

Transport from the cell body to the synapse.

The rapid movement of individual cargoes of both fast and slow components indicates 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. ^ a b c d 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. ^ a b c 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. ^ a b c d 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
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Axoplasmic_transport". A list of authors is available in Wikipedia.
Your browser is not current. Microsoft Internet Explorer 6.0 does not support some functions on Chemie.DE