Where is the axon not insulated with myelin

Repairing and protecting myelin is one of the approaches to treating demyelinating disease like MS. This approach focuses on 1 repairing the damage that has already occurred and 2 preventing further injury to nerves and axons. Several drugs that are currently approved for treating MS follow the second strategy.

They work by suppressing or changing the activity of the immune system, protecting myelin from unwarranted attacks. However, to date none of the available medications address regeneration of lost myelin. Stem cell therapy is one avenue being explored in the search for treatments for MS. These new stem cells were then infused into the spinal cords of mice models of MS where they secreted factors that helped the myelin-producing cells survive.

Consequently, these mice had more myelination and less axonal damage compared to mice that did not receive stem cell infusions. While the results are promising, much more work will need to be done in human clinical trials to determine the therapeutic efficacy.

Continued research efforts funded by public and private institutions worldwide seek to understand how myelin is compromised in diseases like MS, revealing new possibilities for treatment and offering hope to the millions of people affected by these diseases.

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For Educators Log in. Research and Discoveries. Myelin is a fatty material that wraps around nerve cell projections. In this image, myelin can be seen on either end of the nerve fibers.

The gaps in the middle of the fibers are called nodes, which help transmit electrical signals in neurons. Desmazieres, et al. Journal of Neuroscience, In this illustration of a neuron, myelin is shown in yellow. In the nerves outside of the brain and spinal cord, myelin is produced by support cells called Schwann cells.

The nuclei of the Schwann cells are shown here in pink. This image shows a cross-section of a mouse nerve. Myelin, labelled in red, can be seen surrounding the individual nerve cell projections in blue.

Sherman et al. The Journal of Neuroscience, About the Author. Nature Reviews Neuroscience 9, — All rights reserved. Figure Detail What happens if myelin is damaged? The importance of myelin is underscored by the presence of various diseases in which the primary problem is defective myelination.

Demyelination is the condition in which preexisting myelin sheaths are damaged and subsequently lost, and it is one of the leading causes of neurological disease Figure 2.

Primary demyelination can be induced by several mechanisms, including inflammatory or metabolic causes. Myelin defects also occur by genetic abnormalities that affect glial cells. Regardless of its cause, myelin loss causes remarkable nerve dysfunction because nerve conduction can be slowed or blocked, resulting in the damaged information networks between the brain and the body or within the brain itself Figure 3.

Following demyelination, the naked axon can be re-covered by new myelin. This process is called remyelination and is associated with functional recovery Franklin and ffrench-Constant The myelin sheaths generated during remyelination are typically thinner and shorter than those generated during developmental myelination.

In some circumstances, however, remyelination fails, leaving axons and even the entire neuron vulnerable to degeneration. Thus, patients with demyelinating diseases suffer from various neurological symptoms.

The representative demyelinating disease , and perhaps the most well known, is multiple sclerosis MS. This autoimmune neurological disorder is caused by the spreading of demyelinating CNS lesions in the entire brain and over time Siffrin et al. Patients with MS develop various symptoms, including visual loss, cognitive dysfunction, motor weakness, and pain. Approximately 80 percent of patients experience relapse and remitting episodes of neurologic deficits in the early phase of the disease relapse-remitting MS.

There are no clinical deteriorations between two episodes. Approximately ten years after disease onset, about one-half of MS patients suffer from progressive neurological deterioration secondary progressive MS.

About 10—15 percent of patients never experience relapsing-remitting episodes; their neurological status deteriorates continuously without any improvement primary progressive MS. Importantly, the loss of axons and their neurons is a major factor determining long-term disability in patients, although the primary cause of the disease is demyelination.

Several immunodulative therapies are in use to prevent new attacks; however, there is no known cure for MS. Figure 3 Despite the severe outcome and considerable effect of demyelinating diseases on patients' lives and society, little is known about the mechanism by which myelin is disrupted, how axons degenerate after demyelination, or how remyelination can be facilitated. To establish new treatments for demyelinating diseases, a better understanding of myelin biology and pathology is absolutely required.

How do we structure a research effort to elucidate the mechanisms involved in developmental myelination and demyelinating diseases? We need to develop useful models to test drugs or to modify molecular expression in glial cells. One strong strategy is to use a culture system.

Coculture of dorsal root ganglion neurons and Schwann cells can promote efficient myelin formation in vitro Figure 1E. Researchers can modify the molecular expression in Schwann cells, neurons, or both by various methods, including drugs, enzymes, and introducing genes , and can observe the consequences in the culture dish.

Modeling demyelinating disease in laboratory animals is commonly accomplished by treatment with toxins injurious to glial cells such as lysolecithin or cuprizone.

Autoimmune diseases such as MS or autoimmune neuropathies can be reproduced by sensitizing animals with myelin proteins or lipids Figure 3. Some mutant animals with defects in myelin proteins and lipids have been discovered or generated, providing useful disease models for hereditary demyelinating disorders. Further research is required to understand myelin biology and pathology in detail and to establish new treatment strategies for demyelinating neurological disorders.

Myelin can greatly increase the speed of electrical impulses in neurons because it insulates the axon and assembles voltage-gated sodium channel clusters at discrete nodes along its length. Myelin damage causes several neurological diseases, such as multiple sclerosis. Future studies for myelin biology and pathology will provide important clues for establishing new treatments for demyelinating diseases.

Brinkmann, B. Neuron 59 , — Franklin, R. Remyelination in the CNS: From biology to therapy. Nature Reviews Neuroscience 9 , — Nave, K.

Axonal regulation of myelination by neuregulin 1. Current Opinion in Neurobiology 16 , — Poliak, S. The local differentiation of myelinated axons at nodes of Ranvier. Nature Reviews Neuroscience 4 , — Sherman, D. Mechanisms of axon ensheathment and myelin growth. Nature Reviews Neuroscience 6 , — Siffrin, V. Multiple sclerosis — candidate mechanisms underlying CNS atrophy. Trends in Neurosciences 33 , — Susuki, K. Molecular mechanisms of node of Ranvier formation.

Current Opinion in Cell Biology 20 , — Cell Signaling. Ion Channel. Cell Adhesion and Cell Communication. Aging and Cell Division. Endosomes in Plants. Axons are a key element of a neuron since they conduct electrical signals in the form of action potential. Myelin was discovered in the midth century when scientists were observing neurons through a microscope, and they noticed a glistening white substance surrounding the axons.

At the time, it was believed that the myelin was at the core of the axon, however, it was later found to be a substance which wraps around the axons of neurons. This insulation provides protection to these axons in the same way that electrical wires have insulation. Myelin sheath is a low electrical condenser and has high electrical resistance which means it can act as an insulator without disrupting the electrical signals traveling down the axon.

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. Sometimes, as many as revolutions of Schwann cell spirals around the axons of the neurons. Within the CNS, oligodendrocytes are the glia cells which also create myelin sheath. Oligodendrocytes are star-shaped cells which have about 15 arms coming out of their cell body, meaning it is able to myelinate multiple axons at one time.