Why myelin sheath is insulator

Since myelin sheath provides insulation to axons, this allows these axons to conduct electrical signals at a higher speed than if they were not insulated by myelin. Thus, the more thoroughly myelinated an axon is, the higher the speed of electrical transmission. Similarly, myelin sheath around an axon is able to prevent electrical impulses from traveling through the sheath and out of the axon. It prevents the movement of ions into or out of the neuron, also known as depolarization.

This means the current of action potential will only flow down the axon. The more action potential, the more neurons will be able to communicate to each other, transfer electrical and chemical messages, and keep the brain healthy and functioning properly. Whilst the myelin sheath wraps around the axons, there are some small, uncovered gaps between the myelin sheath, which are called the nodes of Ranvier.

These are specialised molecular structures created by the myelin sheath which contains clusters of voltage-sensitive sodium and potassium ion channels. This type of conduction is important for electrical impulses to be formed quickly and means that less energy is required for the conduction of electrical signals.

This is because less energy is needed in myelinated axons to conduct impulses. Myelination is the formation of a myelin sheath, therefore axons which are covered by this insulating sleeve of protection are said to be myelinated axons. If an axon is not surrounded by myelin sheath, it is said to be unmyelinated. The more myelinated axons someone has, the quicker their responses to stimuli will be, due to myelin sheaths increasing the conduction of nerve impulses. Consequently, unmyelinated axons will mean that an individual will not have quicker responses.

Myelin sheath is produced by different types of glia cells. Glia cells are located in the CNS and PNS, that work to maintain homeostasis, and provide support and protection for neurons. The two types of glia cells that produce myelin are Schwann cells and oligodendrocytes. Schwann cells are located within the peripheral nervous system PNS whereas oligodendrocytes are located within the central nervous system CNS.

Schwann cells originate from the neural crest, which is a group of embryonic cells. As such, Schwann cells will first start to myelinate axons during foetal development.

Schwann cells are surrounded by sheets of tissue known as basal lamina. The outside of the basal lamina is covered in a layer of connective tissues known as the endoneurium.

The endoneurium contains blood vessels, macrophages, and fibroblasts. Finally, the inner surface area of the lamina layer faces the plasma membrane of the Schwann cells. For the myelin sheath to be created by Schwann cells in the PNS, the plasma membrane of these cells needs to wrap itself around the axons of the neuron concentrically, spiralling to add membrane layers.

This plasma membrane contains high levels of fat which is essential for the construction of myelin sheath. The cells obtain the other half of the lipids they need from food. Sitting inside the Schwann cells, an enzyme known as fatty acid synthase FASN acts as a central "switch" in the process of synthesising lipids. The team found that this enzyme is essential for the correct composition of lipids in the insulating layers, for the cells to start myelination, and for the healthy growth of myelin layers.

Via the fat molecules produced, called fatty acids, FASN also regulates an entire signal network that plays an important role in myelination. Once this enzyme is missing, the cells can no longer produce critical lipids for the myelin layers. The Schwann cells then rely more heavily on obtaining dietary lipids from blood vessels that pass through nerve fibres. However, Schwann cells laying more far away from the bloodstream can neither synthesise their own lipids nor obtain them well from the blood and therefore cannot insulate the axons sufficiently -- if at all.

In addition, the researcher and her colleagues from various universities, including the Universities of Graz Austria , Washington-St. Louis USA and Zurich, found that even a high-fat diet failed to reverse the process in mice that lacked the enzyme FASN: the axons' insulation remained defective.

This shows that intrinsic lipid production by Schwann cells is essential for the formation of myelin sheaths in the nerves. Montani and her colleagues conducted their experiments using animals with a specific mutation that meant they lacked the enzyme FASN. Her study compared the myelination of these mice with that of mice in which FASN did occur. The study examined animals in their "childhood," from birth onwards, as this is the critical stage of life in which axons receive their myelin insulation.

After adolescence, myelination is more or less complete. This insulation acts to increase the rate of transmission of signals. A gap exists between each myelin sheath cell along the axon. Since fat inhibits the prop agation of electricity, the signals jump from one gap to the next. Multiple sclerosis is characterized by patches of demyelination destruction or loss of the myelin sheath in the central nervous system.

Current Opinion in Cell Biology 20 , — Cell Signaling. Ion Channel. Cell Adhesion and Cell Communication. Aging and Cell Division. Endosomes in Plants. Ephs, Ephrins, and Bidirectional Signaling. Ion Channels and Excitable Cells. Signal Transduction by Adhesion Receptors. Citation: Susuki, K. Nature Education 3 9 How does our nervous system operate so quickly and efficiently?

The answer lies in a membranous structure called myelin. Aa Aa Aa. Information Transmission in the Body. Figure 1. Figure Detail. Axonal Signaling Regulates Myelination. Figure 2: The fate of demyelinated axons. The case in the CNS is illustrated. Research in Myelin Biology and Pathology. Figure 3. References and Recommended Reading Brinkmann, B. Waxman, S. The Axon: Structure, Function and Pathophysiology. New York: Oxford University Press, Article History Close. Share Cancel.

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