An axon is a long, slender projection extending from a nerve cell. Its primary function is to transmit electrical signals, known as action potentials, rapidly over long distances to communicate information to other neurons, muscles, or glands. The speed of this signal—the conduction velocity—determines how quickly an organism can react and process information. Axons wrapped in the specialized fatty myelin sheath transmit these electrical impulses significantly faster than unmyelinated axons.
Understanding Signal Transmission in Unmyelinated Axons
Signal transmission in axons lacking myelin is called continuous conduction. The electrical signal is regenerated continuously along the entire length of the axonal membrane. This regeneration occurs through the sequential opening of voltage-gated ion channels located across the axon surface.
When an action potential occurs, depolarization spreads to the adjacent membrane segment, triggering ion channels to open and refreshing the signal. Since the signal must be re-established along the entire axon, this method is relatively slow, conducting impulses at rates as low as 0.5 to 10 meters per second. This continuous regeneration also requires high energy expenditure to operate the ion pumps that restore ion gradients.
Myelin’s Role as Electrical Insulation
The myelin sheath is composed of a lipid-rich, fatty substance. In the central nervous system, oligodendrocytes form this insulation, while Schwann cells create it in the peripheral nervous system. This multi-layered wrap acts as an effective electrical insulator around the axon.
Myelin fundamentally changes the electrical properties of the axonal membrane by significantly increasing its electrical resistance and decreasing its capacitance. High resistance prevents the flow of ions, meaning the electrical current cannot easily leak out across the membrane. Reducing capacitance allows the electrical force to be carried much faster as an electrical field. Consequently, the electrical signal travels passively and quickly along the insulated segment without needing constant regeneration.
The Mechanism of Saltatory Conduction
The increase in speed is due to the mechanism called saltatory conduction. Myelin forms segments along the axon, separated by tiny, uninsulated gaps known as the Nodes of Ranvier. These nodes are extremely short, typically about one micrometer in length.
The Nodes of Ranvier contain a dense clustering of voltage-gated sodium channels necessary for actively generating an action potential. When the electrical signal reaches a node, the influx of positive sodium ions regenerates the full strength of the action potential. The insulation provided by the myelin sheath then forces the electrical current to flow rapidly down the inside of the axon segment to the next node.
This process creates the appearance of the signal “jumping” from one node to the next, bypassing the entire insulated length. The rapid, passive spread of current under the myelin is quicker than the continuous regeneration required in unmyelinated axons. This mechanism allows myelinated axons to achieve conduction velocities up to 150 meters per second, which can be 10 to 30 times faster than unmyelinated fibers. Because the action potential is only regenerated at the Nodes of Ranvier, the neuron also conserves significant metabolic energy.
Impact of Axon Diameter on Conduction Speed
While myelination is the primary factor driving high-speed conduction, the axon diameter also influences signal velocity. A larger axon diameter increases conduction speed because a wider axon has less internal resistance to the flow of electrical current.
With less resistance, the current travels farther and faster down the axon before it decays. This principle holds true for both unmyelinated and myelinated fibers. Although larger diameter increases speed, the efficiency of myelination still far surpasses the speed advantage gained from diameter alone.

