Axon dysfunction can be the cause of many inherited and acquired neurological disorders that affect both the peripheral and central neurons.

The swollen end of a telodendron is known as the axon terminal or end-foot which joins the dendrite or cell body of another neuron forming a synaptic connection.

A single axon, with all its branches taken together, can target multiple parts of the brain and generate thousands of synaptic terminals.

The longest axons in the human body are those of the sciatic nerve, which run from the base of the spinal cord to the big toe of each foot.

The squid giant axon, which is specialized to conduct signals very rapidly, is close to 1 millimeter in diameter, the size of a small pencil lead.

In comparison, the cerebellar granule cell axon is characterized by a single T-shaped branch node from which two parallel fibers extend.

Elaborate branching allows for the simultaneous transmission of messages to a large number of target neurons within a single region of the brain.

The myelinated axons from the cortical neurons form the bulk of the neural tissue called white matter in the brain.

The myelin gives the white appearance to the tissue in contrast to the grey matter of the cerebral cortex which contains the neuronal cell bodies.

Bundles of myelinated axons make up the nerve tracts in the CNS, and where they cross the midline of the brain to connect opposite regions they are called commissures.

This axonal transport is provided for in the axoplasm by arrangements of microtubules and type IV intermediate filaments known as neurofilaments.

[13] The ion channels are accompanied by a high number of cell adhesion molecules and scaffold proteins that anchor them to the cytoskeleton.

[15] Studies on the axoplasm has shown the movement of numerous vesicles of all sizes to be seen along cytoskeletal filaments – the microtubules, and neurofilaments, in both directions between the axon and its terminals and the cell body.

Afterward, inside the presynaptic terminal, a new set of vesicles is moved into position next to the membrane, ready to be released when the next action potential arrives.

In terms of molecular mechanisms, voltage-gated sodium channels in the axons possess lower threshold and shorter refractory period in response to short-term pulses.

When the UNC-5 netrin receptor is mutated, several neurites are irregularly projected out of neurons and finally a single axon is extended anteriorly.

[37] The ganglioside-converting enzyme plasma membrane ganglioside sialidase (PMGS), which is involved in the activation of TrkA at the tip of neutrites, is required for the elongation of axons.

[38] In addition, exposure to actin-depolimerizing drugs and toxin B (which inactivates Rho-signaling) causes the formation of multiple axons.

Examples of CAMs specific to neural systems include N-CAM, TAG-1 – an axonal glycoprotein[40] – and MAG, all of which are part of the immunoglobulin superfamily.

[42] Nogo-A is a type of neurite outgrowth inhibitory component that is present in the central nervous system myelin membranes (found in an axon).

In recent studies, if Nogo-A is blocked and neutralized, it is possible to induce long-distance axonal regeneration which leads to enhancement of functional recovery in rats and mouse spinal cord.

[46][47][48][49] These studies suggest that motor proteins carry signaling molecules from the soma to the growth cone and vice versa whose concentration oscillates in time with a length-dependent frequency.

The axons of neurons in the human peripheral nervous system can be classified based on their physical features and signal conduction properties.

The first group A, was subdivided into alpha, beta, gamma, and delta fibers – Aα, Aβ, Aγ, and Aδ.

The dysfunction of axons in the nervous system is one of the major causes of many inherited and acquired neurological disorders that affect both peripheral and central neurons.

[64][65] German anatomist Otto Friedrich Karl Deiters is generally credited with the discovery of the axon by distinguishing it from the dendrites.

[5] Swiss Rüdolf Albert von Kölliker and German Robert Remak were the first to identify and characterize the axon initial segment.

Santiago Ramón y Cajal, a Spanish anatomist, proposed that axons were the output components of neurons, describing their functionality.

Alan Hodgkin and Andrew Huxley also employed the squid giant axon (1939) and by 1952 they had obtained a full quantitative description of the ionic basis of the action potential, leading to the formulation of the Hodgkin–Huxley model.

The understanding of the biochemical basis for action potential propagation has advanced further, and includes many details about individual ion channels.