Axoplasmic transport

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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.
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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 (Cowie and Stanton; Sabry et al., 1995). Axonal transport is also responsible for moving molecules destined for degradation from the axon to lysosomes to be broken down (Oztas, 2003). Movement toward the cell body is called retrograde transport and movement toward the synapse is called anterograde transport (Cowie and Stanton).

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[edit] Mechanism

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 (Cowie and Stanton; Karp, 2005).

Mitochondria that are transported along microtubules continue making ATP, which can be used by motor proteins carrying them (Oztas, 2003).

Some evidence suggests that products such as neurofilament subunits can be transported along actin with myosin as a motor (Jung et al., 2004).

[edit] 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; Oztas, 2003). Fast anterograde transport can carry products 100 to 400 millimeters per day (Cowie and Stanton, 2005).

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 (Oztas, 2003). 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 (Cowie and Stanton, 2005; Otzas, 2003).

[edit] 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 (Oztas, 2003). Fast retrograde transport can cover 100-200 millimeters per day (Oztas, 2003).

[edit] 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 (Cowie and Stanton).

[edit] References

  • Cornell. 1998. "Introduction to Neuropathology. Reaction to Injury: Brain Histology." Cornell University Medical College.
  • Cowie R.J. and Stanton G.B. "Axoplasmic Transport and Neuronal Responses to Injury." Howard University College of Medicine.
  • 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.
  • Karp G. 2005. Cell and Molecular Biology: Concepts and Experiments, Fourth ed, p. 344. John Wiley and Sons, Hoboken, NJ.
  • Oztas, E. 2003. Neuronal Tracing. Neuroanatomy. 2: 2-5.
  • Sabry J., O’Connor T. P., and Kirschner M. W. (1995). Axonal Transport of Tuulin in Ti1 Pioneer Neurons in Situ. Neuron. 14: 1247-1256.