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What Is The Purpose Of Myelin Sheath

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Axons are an important component of a neuron, they carry 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 speed of these electrical signals, allowing signals to propagate quickly.

Axons that 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.

Breaking Down The Myelin Sheath. How Adrenomyelopathy Affects The Brain

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 composed of two types of cells: neurons and neuroglia (also known simply as glia or glial cells). Neurons conduct signals throughout the nervous system, while neuroglia provide a supportive structural and metabolic role for neurons by protecting and nourishing neurons, as well as maintaining the surrounding interstitial fluid. That 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 a neuron and neuron types?

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.

Anatomy Qa: Myelin And Neurilemma Sheaths

Myelin is made up of lipids and proteins, a fatty substance with a whitish appearance. It consists of many concentric layers of plasma membrane around the myelin sheath to create 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 to adulthood, with 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 faster their response to stimuli, because myelin sheaths increase the speed of nerve impulses. Think of a baby 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 is still progressing during infancy.

Schwann cells (also called neurolemmocytes) are flat cells that create 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 1 mm of the length of an axon. However, in another arrangement, a Schwann cell may include many (up to 20) unmyelinated axons. In this way, the unmyelinated axons pass through the Schwann cell, but the Schwann cell does not produce a myelin sheath for these axons.

Schwann cells will first begin to myelinate axons during fetal development, wrapping their lipid-rich membrane around them many times until there are multiple layers around the axon. As the wrapping continues, the nucleus and cytoplasm of the Schwann cell are gradually squeezed out. When myelination is complete, the nucleus and cytoplasm of the Schwann cell end up in the outer layer. The myelin sheath itself is the inner part of these wrappings (approximately 100 layers of plasma membrane), and the outer layer that contains the nucleus and cytoplasm is the neurilemma (also called the neurolemma, sheath of Schwann and Schwann’s sheath).

Myelin Plasticity: Sculpting Circuits In Learning And Memory

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 the signal can jump from node to node through the myelin sheath. In unmyelinated axons, the electrical signal travels through any part of the cell membrane which slows down the speed of signal conduction.

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

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 that arise from the cell body. These allow them to 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 thus there is no neurilemma (that is, a cell body and nucleus enclosing an axon) present in oligodendrocytes, unlike in Schwann cells. However, as in Schwann cells, nodes of Ranvier are also present on the axons that are myelinated by oligodendrocytes, but there are much 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 due to a combination of an inhibitory effect on the regrowth of oligodendrocytes and lack of neurolemma.

A Golgi Associated Lipid Kinase Controls Peripheral Nerve Myelination

Since the myelin sheath surrounds the axon, one of its functions is to separate the axon from surrounding extracellular components. However, its main function is to insulate the axon and increase the speed 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 makes it possible for 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 (about 1000 per µm2), while their distribution and numbers under myelin in the internodal axon membrane are sparse. This causes an uneven distribution of ion channels, and the action potential in myelinated axons will “jump” from one node to the next in salt conduction. This type of conduction has important consequences:

The conduction speed of an axon can be linked to its 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 their (diameter)½, while in myelinated axons, the conduction velocity increases linearly. This means that myelinated axons that have the same diameter as unmyelinated axons can conduct signals much faster.

Question Video: Describing The Structure Of The Myelin Sheath

Myelination in the human brain is a continuous process from birth and is not mature until approximately 2 years of age. At this stage, motor and sensory systems are mature and myelination of the cerebral hemispheres is largely complete. However, there are some processes that 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 in the 20s and 30s.

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

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

In the cerebrum, myelination proceeds 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.

Periods Of Synchronized Myelin Changes Shape Brain Function And Plasticity

Now that you are familiar with myelin and myelination,

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