AXON  [ back to Glossary Index ]
Axon is the long, tubular structure at one end of a brain cell, which conducts electric current from the cell body towards the synapse (the junction between adjacent brain cells) when a brain cell is "depolarized" and "fires". Depolarization occurs when receptors on the dendrites of a nerve cell bind with a sufficient amount of excitatory neurotransmitter from adjacent cells to change the ionic balance inside the nerve cell. The axon has no blood supply and cannot nourish itself. Inside the axon are filament shaped microtubules which transport nutrients from the cell body to keep the axon alive. On the outside the axon is made of a cytoskeleon composed largely of calcium, which is wrapped in a protein sheath known as myelin. The myelin acts as an insulation material to speed transmission of electrical current down the axon. Multiple Sclerosis is a highly disabling neurologic disorder involving progressive weakness and paralysis which results from "demyelination," or the the loss of patches of myelin from the axons. ALS (Lou Gerhig's Disease) results from a dying back of the axons resulting in creeping paralysis up the legs to the head. The endpoint of the axon furthest away from the cell body, has small collateral "buds" or "sprouts," each of which ends in a "terminal bouton" that is filled with structures known as "vesicles." The vesicles. resemble tiny bags of of fluid, and are filled with neurotransmitters manufactured in the "body" of the brain cell per instructions of DNA in the nucleus.

When the nerve cell "fires" the mild electric current flows down the axon, and triggers the release of neurotransmitter substances from the vesicles., which then flows into the synapse (nerve junction) and "binds" with receptor sites on the dendrites of dozens, hundred or even thousands of other neurons. There is always excess neurotransmitter substance at the synapse which can be broken down into components parts by an enzyme (such as acetycholinesterase which breaks down acetycholine) or can be siphoned back up into the axonal boutons for later reuse, a process known as "reuptake." Patients with Alzheimer's Disease suffer from memory loss in part because they do not produce enough acetycholine (AcH); hence they are treated with drugs which block the action of acetycholinesterase, which decreases reuptake of AcH and leaves more in the synapse. Prozac improves depression in persons who produce insufficient serotonin, by blocking reuptake of serotonin and leaving a greater supply in the synapses of the the brain cells which regulate mood. Neurotransmitters are classified as excitatory if they cause adjacent brain cells to fire, and as inhibitory if they cause them not to fire. Bunches of axons wrapped in a protein sheath known as endothelium, are what make up large nerve fiber tracts seen in the "white matter" of the brain. The largest of these is the corpus callosum which acts as a nerve fiber "bridge" allowing the left hemisphere (the language center) to communicate with and integrate functions with the right hemisphere (the "spatio-temporal processing" and "motor performance" center).

Trauma to the head which bounces and/or torques the brain, can damage axons in various ways, and damage to the axon will either impair or kill the nerve cell to which it is attached. At very high speed impacts of 70 or 80 mph, the mechanical strain on the axons during head/brain rotation is sufficient to cut through or "shear" millions of axons, which causes death or extremely severe TBI. At much lower speeds of impact, the mechanical strain can bruise the cell membranes and the axons. If the bruising to the cell membranes is sufficient, the "sodium pumps" in the neuron fail, the cell becomes hypersaline, water rushes in and the cells bursts and dies. When the axon is bruised, over the next 24-48 hours the site of the bruise can swell into a "retraction ball" which blocks the flow of nutrients. Through an ongoing cascade of  bio-chemical deterioration, the axon can become split in two or  lose its myelin. Some axons split by gradual biochemical degradation sprouted new buds. Others do not and then die.

The neurochemistry behind these processes is being studied intensively at this time by neuroscience researchers. Individual axons can only be seen in brain tissue removed from a killed organism, placed on a tissue slide, stained and viewed under an electron microscope. MRI is much too weak to visually detect damage to clusters of axons which is associated with "mild" TBI. When a traumatic event produces immediate or delayed destruction of axons, two consequences result which impair brain function. First, there is an imbalance in the production and reuptake of neurotransmitters. Second, this imbalance disturbs the activation and inhibition of brain cells and skews their normal "firing" pattern. Disturbing the release of brain chemicals by mechanical trauma to axons undermines the coordinated firing of brain cells. EEG can detect only faint echoes of dysrhythmic firing because it does not reach deep into the brain, but only picks up signals in the scalp coming through the skull. Microdialysis probes may be used in rats to study local, transient disruptions of neurotransmitter release, but for ethical and medical reasons is not so used in human beings, so the presence of a neurotransmitter imbalance as a result of brain trauma must be inferred from animal research. Technological advances in neuroimaging may allow us one day to measure quantities of neurotransmitters in the brain of a living patient through photographic spectroscopy.