The Myelin Sheath Along an Axon is Not Continuous Between Schwann Cells Are Gaps Called

Myelin sheath and myelination

Author: Alexandra Osika • Reviewer: Francesca Salvador MSc
Last reviewed: October 11, 2022
Reading time: 13 minutes

Axons are a key component of a neuron, they conduct electrical signals in the form of an action potential from the cell body of the neuron to its axon terminal where it synapses with another neuron. An axon is insulated by a myelin sheath throughout its length to increase the velocity of these electrical signals allowing signals to propagate quickly.

Axons which are covered by a myelin sheath, a multilayer of proteins and lipids, are said to be myelinated. If an axon is not surrounded by a myelin sheath, it is unmyelinated. Myelination is the formation of a myelin sheath.

Key facts of the myelin sheath and myelination

Myelination	Produced by Schwann cells for peripheral axons Produced by oligodendrocytes for central axons
Myelin Sheath Function	Insulates axons allowing for rapid action potential conduction Separates axons from surrounding extracellular components
Brain Myelination	Mature at 2 years of age
Clinical Aspects	Demyelination, Schwannoma

This article will discuss the structure and histology of myelin sheaths, their function, and the process of brain myelination.

Contents

1. Overview
2. Myelination
   1. Myelin
   2. Schwann cells
   3. Oligodendrocytes
3. Myelin sheath function
4. Brain myelination
5. Clinical aspects
   1. Demyelination
   2. Schwannoma
6. Sources

+ Show all

Overview

To understand myelination, we must first understand the cellular structure of the nervous system. Recall that the nervous system is composed of two types of cells: neurons and neuroglia (also simply known as glia or glial cells). Neurons conduct signals throughout the nervous system, while neuroglia provide a supporting structural and metabolic role for neurons by protecting and nourishing neurons, as well as maintaining the surrounding interstitial fluid. This is why they are known as the "glue" of the nervous system ("glia" is Greek for "glue").

Each neuron has four specialized regions to perform different functions:

• Dendrites receive incoming information. They are part of the receptive segment of a neuron.
• The cell body (also called soma or perikaryon) also receives incoming information and integrates information together. Depending on the type of neuron, various extensions or processes will extend from the cell body such as dendrites and an axon. As the cell body receives information, it is part of the receptive segment of a neuron.
• The axon then conducts information from the cell body of a neuron to the axon terminal. An axon makes up the conductive segment of a neuron.
• Axon terminals are the presynaptic component of a synapse, the site of intercellular communication, where a neuron transmits its signal to another neuron. Axon terminals are the transmissive segment of a neuron.

It is the axon of a neuron which is myelinated.

Before you go any further, why not test how well you know the different parts of a neuron and neuron types?

Myelination

Myelination is the formation of a myelin sheath.  Myelin sheaths are made of myelin, and myelin is produced by different types of neuroglia: oligodendrocytes and Schwann cells, where oligodendrocytes myelinate axons in the central nervous system, and Schwann cells myelinate axons in the peripheral nervous system. So which cells form myelin in the spinal cord? Since the spinal cord is part of the central nervous system, oligodendrocytes form this myelin. Functionally, oligodendrocytes and Schwann cells perform the same role, but structurally they are different.

Remember these cells and their location with the mnemonic "COPS" (Central - Oligodendrocytes, Peripheral - Schwann).

Myelin

Myelin is made up of lipids and proteins, a fatty substance with a whitish appearance. It is made up of many concentric layers of plasma membrane to make up the myelin sheath around axons. Myelin sheath and myelin function are therefore the same, to increase the speed of nerve impulses.

The amount of myelin in the body increases throughout development, from fetal development up until maturity, with the myelination in the prefrontal cortex being the last to complete in the 2nd or 3rd decade. The more myelin and myelination an individual has, the quicker their response is to stimuli because myelin sheaths increase the speed of nerve impulses. Think of a baby that is still learning to walk– their response to stimuli is slow and uncoordinated compared to a child, teenager, or adult. This is partly because myelination of axons during infancy is still progressing.

Schwann cells

Schwann cells (also known as neurolemmocytes) are flat cells which make up myelin sheaths on axons of the peripheral nervous system. Each Schwann cell myelinates only one axon, where one peripheral axon will have multiple Schwann cells myelinating its length as one Schwann cell wraps a lipid-rich membrane layer around approximately 1 mm of an axon's length. However, in a different arrangement, a Schwann cell can enclose many (up to 20) unmyelinated axons. In this way, the unmyelinated axons go through the Schwann cell, but the Schwann cell does not produce a myelin sheath for these axons.

Schwann cells will first start to myelinate axons during fetal development, wrapping its lipid-rich membrane around it many times until there are multiple layers surrounding the axon. As the wrapping continues, the nucleus and cytoplasm of the Schwann cell are gradually squeezed out. Once myelination is complete, the Schwann cell's nucleus and cytoplasm finish in the outermost layer. The myelin sheath itself is the inner portion of these wrappings (approximately 100 layers of plasma membrane), and the outermost layer that contains the nucleus and cytoplasm is the neurilemma (also called the neurolemma, sheath of Schwann, and Schwann's sheath).

Along an axon, there are gaps between Schwann cells and the myelin sheath called the nodes of Ranvier. Here, electrical impulses are formed more quickly and allow the signal to jump from node to node through the myelin sheath. In unmyelinated axons, the electrical signal travels through each part of the cell membrane which slows the speed of signal conduction.

Schwann cells also play a role in forming connective tissue sheaths in neuron development and axon regeneration, providing chemical and structural support to neurons. The neurilemma assists in regeneration of an axon when it is damaged by forming a regeneration tube to stimulate and guide its regeneration.

Oligodendrocytes

Oligodendrocytes (or oligodendroglia) are star-shaped neuroglia that form the myelin sheaths on axons of the central nervous system. A single oligodendrocyte has about 15 flat, broad, arm-like processes coming out of the cell body. With these they can myelinate multiple axons by spiraling around them to form a myelin sheath. The cell body and nucleus of oligodendrocytes remain separate from the myelin sheath, and so there is no neurilemma (that is, a cell body and nucleus enveloping an axon) present in oligodendrocytes, unlike in Schwann cells. However, like in Schwann cells, nodes of Ranvier are also present on the axons myelinated by oligodendrocytes, but there are far fewer of them.

Once an axon in the central nervous system is injured, there is little regrowth unlike axons in the peripheral nervous system. It is uncertain why this is but it is thought to be because of a combination of an inhibitory influence on regrowth from oligodendrocytes and lack of neurolemma.

Myelin sheath function

Since the myelin sheath surrounds the axon, one of its functions is to separate the axon from surrounding extracellular components. Its main function, however, is to insulate the axon and  increase the velocity of action potential propagation.

Myelin has properties of low capacitance and high electrical resistance which means it can act as an insulator. Therefore, myelin sheaths insulate axons to increase the speed of electrical signal conduction. This allows myelinated axons to conduct electrical signals at high speeds.

Nodes of Ranvier (gaps in myelination) contain clusters of voltage-sensitive sodium and potassium ion channels (approximately 1000 per µm2) whereas their distribution and numbers under myelin in the internodal axon membrane are spare. This creates an uneven distribution of ion channels, and the action potential in myelinated axons will "leap" from one node to the next in saltatory conduction. This type of conduction has important consequences:

• Increased conduction velocity
• Reduced metabolic cost of conduction as the amount of energy needed in myelinated fibers to conduct the impulse is less

The conduction velocity of an axon can be linked to the diameter. Myelinated axons are quite large in diameter, ranging from 1 - 13 µm. Unmyelinated axons on the other hand have a small diameter– generally less than 0.2 µm in the central nervous system and less than 1 µm in the peripheral nervous system. In unmyelinated axons, the conduction velocity is proportional to its (diameter)½ while the conduction velocity in myelinated axons increases linearly. This means that myelinated axons that are the same diameter as unmyelinated axons can conduct signals much faster.

Brain myelination

Myelination in the human brain is a continuous process from birth and is not mature until about 2 years of age. At this stage, motor and sensory systems are mature and myelination of the cerebral hemispheres is largely complete. There are, however, some processes which myelinate later in life: some thalamic radiations will be mature at about 5 - 7 years of age; and myelination of intracortical connections between association cortices continues into the 20s and 30s.

Brain myelination begins in utero, developing quite prominently from the 24th week of gestation. At birth, the myelination process continues to progress, and completes at about 2 years of age. It's progression is predictable, and correlates with developmental milestones such as learning to walk.

Throughout the first year of life, myelin will spread throughout the whole brain in an orderly manner. Generally, myelination will start in the brainstem and progress to the cerebellum and basal ganglia, then will continue rostrally to the cerebrum, and rostrally from the occipital and parietal lobes to the frontal and temporal lobes. The progression typically follows the order from central to peripheral, caudal to rostral (inferior to superior), and dorsal to ventral (posterior to anterior).

In the cerebrum, myelination progresses from the lower order cortices to higher order cortices. Primary cortical areas such as the primary motor cortex myelinate first, followed by secondary cortices, such as the premotor and supplementary motor cortices, and finally tertiary cortical areas such as the prefrontal cortex.

Now that you are familiar with myelin and myelination, why not take a broader look at histology of structures of nervous tissue via our fully customisable quiz!

Clinical aspects

Demyelination

Myelin sheaths around an axon can be destroyed or lost in demyelination. This may lead to a deterioration of the nerve because of the loss of myelin protecting the axon. It can be caused by various disorders like Tay-Sachs or multiple sclerosis and also by damaging medical treatments like chemotherapy and radiotherapy.

Schwannoma

A Schwannoma (neurilemmoma) is a benign peripheral nerve tumor that originates from Schwann cells. These tumors are most commonly found in the head and neck region. When a tumor arises from the vestibulocochlear nerve (CN VIII), it is known as an acoustic neuroma. It usually occurs in the middle years of life and interferes with the function of the cochlear root of the vestibulocochlear nerve– impairing hearing, causing unilateral hearing loss, and sometimes symptoms of tinnitus. If the tumor expands into the internal acoustic meatus, function of the facial nerve (CN VII) can also be affected, as the facial nerve runs adjacent to the vestibulocochlear nerve in the internal acoustic meatus. This can result in facial paralysis, swallowing difficulty, and a loss of sensation in the face. Schwannomas are typically treated by surgical removal with an excellent prognosis in most cases.

Sources

All content published on Kenhub is reviewed by medical and anatomy experts. The information we provide is grounded on academic literature and peer-reviewed research. Kenhub does not provide medical advice. You can learn more about our content creation and review standards by reading our content quality guidelines.

References:

• Diepenbrock, N.H. (2012) Schwannoma. In Quick Reference To Critical Care. (2011). Wolters Kluwer Health, Lippincott Williams & Wilkins.
• Martin, J. H. (2012). Neuroanatomy: Text and Atlas (4th ed.). New York: McGraw-Hill Medical.
• Rapp, Peter R., & Bachevalier, Jocelyne. (2013). Chapter 43 - Cognitive Development and Aging. In Fundamental Neuroscience (pp. 919–945). Retrieved from https://doi.org/10.1016/B978-0-12-385870-2.00043-3
• Ross, M. H., & Pawlina, W. (2011). Histology: A Text and Atlas (6th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.
• Tortora, G. J., & Nielsen, M. (2014). Principles of Human Anatomy (13th ed.). Hoboken, NJ: Wiley.
• Waxman, S. G. (2010). Clinical neuroanatomy (26th ed.). New York: McGraw-Hill.

Article, review and layout:

• Alexandra Osika
• Francesca Salvador
• Jana Vaskovic

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