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What Is The Function Of Myelin In Nerve Cells

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What Is The Function Of Myelin In Nerve Cells

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Axons are the main components of a neuron, they conduct electrical signals in the form of action potentials from the neuron’s cell body to its axon terminal where it synapses with another neuron. The axon is insulated throughout its length by a Myelin sheath to speed up these electrical signals so that the signal can travel faster.

Axons covered by a multi-layered, Myelin Sheath of proteins and lipids are called myelinated. If an axon is not surrounded by a myelin sheath, it is amylinized. Myelination is the formation of a myelin sheath.

What Is Myelin?

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

To understand myelination, we must first understand the cellular structure of the nervous system. Remember that the nervous system is made up of two types of cells: neurons and neuroglia (also called glia or glial cells). Neurons conduct signals throughout the nervous system, while neuroglia provide basic structural and metabolic roles 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”).

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

Myelination is the formation of a myelin sheath. Myelin sheaths are composed 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 in the spinal cord produce myelin? Since the spinal cord is part of the central nervous system, oligodendrocytes produce myelin. Functionally, oligodendrocytes and Schwann cells play similar roles, but structurally they are different.

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Myelin is composed of lipids and proteins, a fatty substance that is white in color. It is composed of several concentric layers of plasma membrane to form a myelin sheath around the axon. So the function of myelin sheath and myelin to speed up nerve impulses is similar.

The amount of myelin in the body increases throughout development from fetal development to adulthood, with myelination in the prefrontal cortex being the last to be completed in the second or third decade. The more myelin and myelination a person has, the faster their stimulus response is because myelin sheaths increase the speed of nerve impulses. Think of a baby who is still learning to walk—their response to stimuli is slow and uncoordinated compared to that of a toddler, teenager, or adult. This is partly because myelination of axons is still progressing during infancy.

Schwann cells (also known as neurolymocytes) are flat cells that form the myelin sheath on the axons of the peripheral nervous system. Each Schwann cell myelinates only one axon, whereas a peripheral axon contains many Schwann cells that are myelinated because a Schwann cell wraps a layer of lipid-rich membrane about 1 mm along the length of the axon. However, in a different arrangement, a Schwann cell can terminate many (up to 20) amyelinated axons. Thus, unmyelinated axons pass through the Schwann cell, but the Schwann cell does not produce a myelin sheath for these axons.

Schwann cells first begin to myelinate the axon during embryonic development, wrapping several times around its lipid-rich membrane until several layers surround the axon. As coiling continues, the nucleus and cytoplasm of the Schwann cell are gradually squeezed. When myelination is complete, the Schwann cell’s nucleus and cytoplasm end up in the outermost layer. The myelin sheath itself is the inner part of these sheaths (approximately 100 layers of plasma membrane), and the outermost layer, which contains the nucleus and cytoplasm, is the neurilemma (also called neurolemma, Schwann’s sheath, and Schwann’s sheath).

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

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

Oligodendrocytes (or oligodendroglia) are star-shaped neuroglia that form the myelin sheath on central nervous system axons. An oligodendrocyte has about 15 flat, broad, arm-like processes protruding from the cell body. With this 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 therefore oligodendrocytes do not have a neurilemma (i.e. the cell body and nucleus covering the axon), unlike Schwann cells. However, like Schwann cells, axons myelinated by oligodendrocytes also have nodes of Ranvier, but there are very few of them.

Once an axon in the central nervous system is injured, there is little growth in contrast to axons in the peripheral nervous system. Why this is is uncertain but is thought to be due to the inhibitory effect on regeneration of oligodendrocytes and the lack of neurolemma.

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Since the axon is surrounded by a myelin sheath, one of its functions is to isolate the axon from the surrounding environment. However, its main function is to depolarize axons and increase the speed of action potential propagation.

Myelin has low capacitance and high electrical resistance properties 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 of myelination) contain clusters (approximately 1000 per µm2) of voltage-sensitive sodium and potassium ion channels, while their distribution and number within the myelin in the internodal axon membrane is redundant. This creates an uneven distribution of ion channels and action potentials in myelinated axons “jump” from one node to another. This type of conduction has important consequences:

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

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Myelination in the human brain is a continuous process from birth and does not mature until about 2 years of age. At this stage, the motor and sensory systems are mature and myelination of the cerebral hemispheres is largely complete. However, there are processes that become myelinated later in life: some thalamic radiations will mature at 5 – 7 years of age; and myelination of intracortical connections in the association cortices begins in the 20s and 30s.

Myelination of the brain begins in utero, developing prominently from the 24th week of gestation. At birth, the myelination process continues to progress and is complete by age 2. Its progress is predictable, and correlates with developmental milestones such as learning to walk.

During the first year of life, myelin spreads smoothly throughout the brain. Generally, myelination will begin in the brainstem and progress to the cerebellum and basal ganglia, then continue rostrally to the cerebrum and continue rostrally from the occipital and parietal lobes to the frontal and temporal lobes. Progression is generally in the order central to peripheral, caudal to rostral (inferior to superior), and dorsal to ventral (posterior to anterior).

In the cerebrum, myelination progresses from 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.

Learn More About Ms And The Myelin Sheath

Now that you are familiar with myelin and myelination,

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