For most of the topics only Differences and Similarities are given. No thorough information on topics is given. Thank you Amit KUmar for your comment. It is for degree or higher secondary students. For cracking the CSIR examination you need thorough understanding about the concept.
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. 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 , — How do nodes of Ranvier speed up conduction? Nodes of Ranvier. Nodes of Ranvier are microscopic gaps found within myelinated axons. Their function is to speed up propagation of action potentials along the axon via saltatory conduction. The Nodes of Ranvier are the gaps between the myelin insulation of Schwann cells which insulate the axon of neuron.
How does myelin speed up signal transmission? Most nerve fibres are surrounded by an insulating, fatty sheath called myelin, which acts to speed up impulses. The myelin sheath contains periodic breaks called nodes of Ranvier.
By jumping from node to node, the impulse can travel much more quickly than if it had to travel along the entire length of the nerve fibre. Why does increasing the axon diameter increase the speed of impulse conduction? Why do action potentials travel faster in myelinated axons?
The speed of action potential conduction is faster in myelinated axons, like I've drawn here with the myelin sheath in yellow, because the capacitance of the membrane is reduced in the myelinated segments, which decreases the number of ions and the time needed to change the membrane potential in these areas.
Why are axons not completely wrapped in myelin? With no myelin, the action potential must travel down the length of the axon, like a string of dominoes being knocked over. With myelin, the action potential can 'leapfrog' between the nodes of Ranvier, travelling much faster, since it only has to move along the membrane for short distances.
What happens when an action potential reaches the axon terminal? Which nerves are Unmyelinated? The C group fibers are unmyelinated and have a small diameter and low conduction velocity, whereas Groups A and B are myelinated. Group C fibers include postganglionic fibers in the autonomic nervous system ANS , and nerve fibers at the dorsal roots IV fiber. These fibers carry sensory information.
0コメント