Neurons possess unique capabilities in controlling and responding to electricity. Their response and control mechanisms differ in each part of the neuron due to its distinct morphology and ion channel composition. Dendrites, for example, have ligand-gated ion channels that enable responses to chemicals released by other neurons, while their branching pattern facilitates integration of multiple input signals. On the other hand, axons are characterized by their long length and high concentration of voltage-gated channels, allowing them to rapidly transmit electrical signals (action potentials) over long distances without modification.

Since the soma serves as the metabolic center of the neuron, it synthesizes substances necessary to support the functioning of axons and synapses. However, distributing these substances to replenish depleted or inactivated materials along the axon and especially in the presynaptic terminals is a challenge due to the inefficient diffusion over long distances. To address this, specialized axonal transport mechanisms have evolved (Fig. 4.3).

Axons degenerate when separated from the cell body, which has been utilized by scientists to trace neuronal pathways. By cutting an axonal pathway, researchers can determine the projections of degenerating axons distal to the cut.

There are various types of axonal transport. Fast axonal transport allows for the rapid movement of membrane-bound organelles and mitochondria, while slow axonal transport is responsible for transporting dissolved substances such as proteins. In mammals, fast axonal transport can reach speeds of up to 400 mm/day, whereas slow axonal transport occurs at approximately 1 mm/day. For example, synaptic vesicles, which undergo fast axonal transport, can travel from the soma of a motor neuron in the spinal cord to a neuromuscular junction in a person's foot in approximately 2.5 days. Conversely, the movement of certain soluble proteins over the same distance may take nearly 3 years.

Axonal transport requires metabolic energy and involves calcium ions. Microtubules act as guiding structures along which membrane-bound organelles travel, similar to the linkage between thick and thin filaments in skeletal muscle fibers. The movement of organelles along microtubules is triggered by Ca++. Axonal transport relies on specific microtubule-associated motor proteins called kinesin and dynein.

Axonal transport occurs in both anterograde and retrograde directions. Anterograde axonal transport, driven by kinesin, facilitates the replenishment of synaptic vesicles and the synthesis of neurotransmitters in synaptic terminals. Retrograde axonal transport, powered by dynein, transports recycled synaptic vesicle membrane back to the soma for lysosomal degradation.
CHAPTER 4 The Nervous System: Introduction to Cells and Systems •Fig. 4.3 Axonaltransport.Schematicofneuronandenlargementofaxonaltransportmechanism.Axonaltransportdependsonmovementofmaterialalongtransportfilamentssuchasmicrotubules.Transportedcomponentsattachtotransportfilamentsbymeansofcross-bridges.Differentobjectsaretransportedanterogradely(fromcellbodytoaxonterminal)andothersretrogradely(towardthecellbody).Thedirectionoftransport—retrogradeandanterograde—isdeterminedbyspecificproteinssuch asdyneinandkinesin,respectively.
Neurons are special because of their ability to control and respond to electricity. Moreover, the response and control mechanisms of each part of a neuron are distinct from those in other parts. This intraneuronal specialization is a consequence of the particular morphology and the ion channel composition of each part of the neuron. For example, dendrites have ligand gated ion channels that allow neurons to respond to chemicals released by other neurons, and their characteristic branching pattern allows for integration of multiple input signals. In contrast the axon typically has a long length and high concentration of voltage-gated channels that allows it to convey electrical signals (action potentials) rapidly over long distances without alteration.
Because the soma is the metabolic engine of the neuron, substances needed to support axonal and synaptic function are synthesized there. These substances must be distributed to replenish secreted or inactivated materials along the axon and especially to the presynaptic terminals. Most axons are too long to allow efficient movement of substances from the soma to the synaptic endings by simple diffusion. Thus special axonal transport mechanisms have evolved to accomplish this task (
Fig. 4.3).
A consequence of this metabolic dependency is that axons degenerate when disconnected from the cell body, a fact that has been used by scientists tracing out neuronal pathways; they would cut an axonal pathway and then determine where the degenerating axons distal to the cut projected to.
Several types of axonal transport exist. Membrane-bound organelles and mitochondria are transported relatively rapidly by fast axonal transport. Substances that are dissolved in cytoplasm (e.g., proteins) are moved by slow axonal transport. In mammals, fast axonal transport proceeds as rapidly as 400 mm/day, whereas slow axonal transport occurs at about 1 mm/day. Synaptic vesicles, which travel by fast axonal transport, can travel from the soma of a motor neuron in the spinal cord to a neuromuscular junction in a person’s foot in about 2.5 days. In comparison the movement of some soluble proteins over the same distance can take nearly 3 years.
Axonal transport requires metabolic energy and involves calcium ions. Microtubules provide a system of guidewires along which membrane-bound organelles move (see
Fig.
4.3 ). Organelles attach to microtubules through a linkage similar to that between the thick and thin filaments of skeletal muscle fibers. Ca++ triggers movement of the organelles along the microtubules. Special microtubule-associated motor proteins called kinesin and dynein are required for axonal transport.
Axonal transport occurs in both directions. Transport from the soma toward the axonal terminals is called anterograde axonal transport. This process involves kinesin, and it allows replenishment of synaptic vesicles and enzymes responsible for the synthesis of neurotransmitters in synaptic terminals. Transport in the opposite direction, which is driven by dynein, is called retrograde axonal transport. This process returns recycled synaptic vesicle membrane to the soma for lysosomal degradation.