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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. Axonal transport is also responsible for moving molecules destined for degradation from the axon to lysosomes to be broken down. Movement toward the cell body is called retrograde transport and movement toward the synapse is called anterograde transport.
Microtubules, or neurotubules, lie along the axis of the axon. The motor proteins kinesin and dynein, which change their shape in the presence of adenosine triphosphate, inch up and down microtubules. The motor proteins bind and can carry anything from large molecules like RNA and cytoskeletal building blocks, to organelles such as ribosomes, to vesicles with products like neurotransmitters packaged into them.
Mitochondria that are transported along microtubules continue making ATP, which can be used by motor proteins carrying them.
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). Fast anterograde transport can carry products 100 to 400 millimeters per day.
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. 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.
Retrograde transport, which is mediated by dynein, sends chemical messages, and endocytosis products headed to endolysosomes from the axon back to the cell. Fast retrograde transport can cover 100-200 millimeters per day.
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.
- ↑ 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.
- ↑ 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.
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 Oztas E. 2003. Neuronal Tracing. Neuroanatomy. 2: 2-5. Retrieved on January 25, 2007.
- ↑ Karp G. 2005. Cell and Molecular Biology: Concepts and Experiments, Fourth ed, p. 344. John Wiley and Sons, Hoboken, NJ. ISBN 0471465801
- ↑ Jung C., Chylinski T. M., Pimenta A., Ortiz D., and Shea T. B. 2004. Neurofilament transport is dependent on actin and myosin. Journal of Neuroscience 24(43): 9486-9496. PMID 15509735. Retrieved on January 25, 2007.
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