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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 (made of tubulin) run along the length of the axon and provide the main cytoskeletal "tracks" for transportation. The motor proteins kinesin and dynein are mechanochemical enzymes that move cargoes in the anterograde (towards the axon tip) and retrograde (towards the cell body) directions, respectively. Motor proteins bind and transport several different cargoes including organelles such as mitochondria, cytoskeletal polymers, and vesicles containing neurotransmitters.[1]

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.[4] Fluorescent labeling techniques (e.g. fluorescence microscopy) have enabled direct visualization of transport in living neurons. (See also: Anterograde tracing.)

Anterograde transport[]

Axonal transport can be divided into anterograde and retrograde categories and further divided into fast and slow subtypes. Anterograde transport, mediated by kinesin, carries products like organelles and substances for making neurotransmitters away from the cell body toward the plus end of microtubules (toward the synapse).[3] Fast anterograde transport can carry products 100 to 400 millimeters per day.[1]

There are two types of slow anterograde transport: type slow A can carry products 0.1 millimeter per day, and slow B can carry them at a rate of up to six millimeters a day.[3] Slow anterograde transport, which is responsible for the movement of enzymes and cellular products like tubulin, the building blocks for microtubules, is used for repair and replacement of cytoskeleton subunits.[1][3]

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.

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 1.4 1.5 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 Tuulin 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 3.3 3.4 3.5 Oztas E. 2003. Neuronal Tracing. Neuroanatomy. 2: 2-5. Retrieved on January 25, 2007.
  4. Cite error: Invalid <ref> tag; no text was provided for refs named Roy
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