• what is the difference between myelinated and unmyelinated axons

The C fibers of the skin, muscles, and viscera are also unmyelinated fibers. The olfactory nerves are also unmyelinated. Figure 2: Myelinated and Unmyelinated Nerve Fibers. Unmyelinated nerve fibers contain Swann cells as a series on the nerve fiber. But, these Schwann cells do not spiral the mesaxon around the nerve fiber. The endoneurium encloses a single layer of the Schwann cells.

Both myelinated and unmyelinated nerve fibers are shown in figure 2. Myelinated Nerve Fibers: Myelinated nerve fibers are the nerve fibers that are insulated by a myelin sheath, allowing the faster conduction of the action potential along the nerve fiber.

Unmyelinated Nerve Fibers: Unmyelinated nerve fibers are the nerve fibers that do not have a myelin sheath. Myelinated Nerve Fibers: Myelinated nerve fibers contain a myelin sheath around the nerve fiber. Unmyelinated Nerve Fibers: Unmyelinated nerve fibers do not contain a myelin sheath. Myelinated Nerve Fibers: The myelinated nerve fibers are white in color. Unmyelinated Nerve Fibers: The unmyelinated nerve fibers are gray in color.

Myelinated Nerve Fibers: The myelinated nerve fibers consist of nodes of Ranvier. Unmyelinated Nerve Fibers: The unmyelinated nerve fibers do not consist of nodes of Ranvier.

Myelinated Nerve Fibers: Since transmission occurs only through nodes of Ranvier, the speed of transmission of nerve impulses is high in myelinated nerve fibers. Neurons are the building blocks or the basic cells of the nervous system. Neurons are responsible for transmitting the right information or command to correct location of the body.

A neuron has three main components: cell body, dendrites, and an axon. Dendrites receive electrical signal and handover to the axon. Axon transmits the signal to the next neuron. Axons are insulated with an electrical insulator layer called myelin sheath. Myelin sheath is composed of a fatty material called myelin. Myelin sheath is produced by special peripheral nervous system cells called Schwann cells. Myelin is produced by Schwann cells, and myelin sheath is formed around the axon in a spiral fashion.

Myelin sheath increases the speed of the signal transmission, but not all axons are myelinated. Based on the presence and absence of the myelin sheath around the axon, there are two types of neurons. They are myelinated neurons and unmyelinated neurons. Myelinated neurons possess myelinated axons, and unmyelinated neurons possess unmyelinated axons. The key difference between myelinated axon and unmyelinated axon is that myelinated axons have a myelin sheath while unmyelinated axons do not have a myelin sheath.

Overview and Key Difference 2. What are Myelinated Axons 3. What are Unmyelinated Axons 4. Collateral fibres are not produced in unmyelinated nerves.

For most of the topics only Differences and Similarities are given. No thorough information on topics is given. One mechanism has been identified in PNS myelination. Unmyelinated autonomic neurons express low levels of neuregulin 1 type III on the axon surface, whereas heavily myelinated axons express high levels. Without neuregulin 1 type III, Schwann cells in culture derived from these mutant mice cannot myelinate neurons in the spinal cord dorsal root ganglion neurons.

Intriguingly, in normally unmyelinated fibers, forced expression of neuregulin 1 type III in the postganglionic fibers of sympathetic neurons grown in culture can be forced to myelinate. Furthermore, above the threshold, the myelin formation is correlated with the amount of neuregulin 1 type III presented by the axon to the Schwann cell. Reduced expression of neuregulin 1 type III leads to a thinner than normal myelin sheath in the heterozygous mutant mice of this molecule.

In contrast, transgenic mice that overexpress neuregulin 1 become hypermyelinated. Although several reports show that oligodendrocytes respond to neuregulin 1 in vitro, analyses of a series of conditional null mutant animals lacking neuregulin 1 showed normal myelination Brinkmann et al.

It is still unclear how myelination is regulated in the CNS. How does myelin enhance the speed of action potential propagation? It insulates the axon and assembles specialized molecular structure at the nodes of Ranvier. In unmyelinated axons, the action potential travels continuously along the axons.

For example, in unmyelinated C fibers that conduct pain or temperature 0. In contrast, among the myelinated nerve fibers, axons are mostly covered by myelin sheaths, and transmembrane currents can only occur at the nodes of Ranvier where the axonal membrane is exposed.

At nodes, voltage-gated sodium channels are highly accumulated and are responsible for the generation of action potentials. The myelin helps assemble this nodal molecular organization.

For example, during the development of PNS myelinated nerve fibers, a molecule called gliomedin is secreted from myelinating Schwann cells then incorporated into the extracellular matrix surrounding nodes, where it promotes assembly of nodal axonal molecules. Due to the presence of the insulating myelin sheath at internodes and voltage-gated sodium channels at nodes, the action potential in myelinated nerve fibers jumps from one node to the next.

This mode of travel by the action potential is called "saltatory conduction" and allows for rapid impulse propagation Figure 1A. Following demyelination, a demyelinated axon has two possible fates. The normal response to demyelination, at least in most experimental models, is spontaneous remyelination involving the generation of new oligodendrocytes.

In some circumstances, remyelination fails, leaving the axons and even the entire neuron vulnerable to degeneration. Remyelination in the CNS: from biology to therapy. 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.