query: the cells that surround an axon creating a myelin sheath in the pns are called

pos: Myelin recorded conduction speed (across both vertebrates and invertebrates) is found in the ensheathed axons of the Kuruma shrimp, an invertebrate, ranging between 90 and 200 m/s (cf 100–120 m/s for the fastest myelinated vertebrate axon.) Myelin Myelin is a lipid-rich (fatty) substance formed in the central nervous system (CNS) by glial cells called oligodendrocytes, and in the peripheral nervous system (PNS) by Schwann cells. Myelin insulates nerve cell axons to increase the speed at which information (encoded as an electrical signal) travels from one nerve cell body to another (as in the CNS) or, for example, from a nerve cell

pos: Myelin incisure Myelin incisure Myelin incisures (a.k.a. Schmidt-Lanterman clefts, Schmidt-Lanterman incisures, clefts of Schmidt-Lanterman, segments of Lanterman, medullary segments), are small pockets of cytoplasm left behind during the Schwann cell myelination process. They are histological evidence of the small amount of cytoplasm that remains in the inner layer of the myelin sheath created by Schwann cells wrapping tightly around an axon (nerve fiber). In the peripheral nervous system (PNS) axons can be either myelinated or unmyelinated. Myelination refers to the insulation of an axon with concentric surrounding layers of lipid membrane (myelin) produced by Schwann cells. These layers are generally uniform and

pos: Myelin incisure initially around only part of its circumference. Secondary incisures appear later, in regions of a compact myelin sheath, initially traversing only part of its radial thickness but commonly occupying its whole circumference. Myelin incisure Myelin incisures (a.k.a. Schmidt-Lanterman clefts, Schmidt-Lanterman incisures, clefts of Schmidt-Lanterman, segments of Lanterman, medullary segments), are small pockets of cytoplasm left behind during the Schwann cell myelination process. They are histological evidence of the small amount of cytoplasm that remains in the inner layer of the myelin sheath created by Schwann cells wrapping tightly around an axon (nerve fiber). In the peripheral nervous system (PNS) axons

pos: Myelin Myelin Myelin is a lipid-rich (fatty) substance formed in the central nervous system (CNS) by glial cells called oligodendrocytes, and in the peripheral nervous system (PNS) by Schwann cells. Myelin insulates nerve cell axons to increase the speed at which information (encoded as an electrical signal) travels from one nerve cell body to another (as in the CNS) or, for example, from a nerve cell body to a muscle (as in the PNS). The myelinated axon can be likened to an electrical wire (the axon) with insulating material (myelin) around it. However, unlike the plastic covering on an electrical wire,

pos: Node of Ranvier of the action potential. Many vertebrate axons are surrounded by a myelin sheath, allowing rapid and efficient saltatory ("jumping") propagation of action potentials. The contacts between neurons and glial cells display a very high level of spatial and temporal organization in myelinated fibers. The myelinating glial cells; oligodendrocytes in the central nervous system (CNS), and Schwann cells in the peripheral nervous system (PNS), are wrapped around the axon, leaving the axolemma relatively uncovered at the regularly spaced nodes of Ranvier. The internodal glial membranes are fused to form compact myelin, whereas the cytoplasm-filled paranodal loops of myelinating cells are spirally

pos: Oligodendrocyte Oligodendrocyte Oligodendrocytes (), or oligodendroglia, are a type of neuroglia discovered by Pío del Río Hortega. Their main functions are to provide support and insulation to axons in the central nervous system of some vertebrates, equivalent to the function performed by Schwann cells in the peripheral nervous system. Oligodendrocytes do this by creating the myelin sheath, which is 80% lipid and 20% protein. A single oligodendrocyte can extend its processes to 50 axons, wrapping approximately 1 μm of myelin sheath around each axon; Schwann cells, on the other hand, can wrap around only one axon. Each oligodendrocyte forms one segment

pos: Glia earlier developmental state to encourage regrowth of the axon. This difference between the CNS and the PNS, raises hopes for the regeneration of nervous tissue in the CNS. For example, a spinal cord may be able to be repaired following injury or severance. Schwann cells are also known as neuri-lemmocytes. These cells envelop nerve fibers of the PNS by winding repeatedly around a nerve fiber with the nucleus inside of it. This process creates a myelin sheath, which not only aids in conductivity but also assists in the regeneration of damaged fibers. Oligodendrocytes are another type of glial cell of

pos: Axon different sets of motor proteins. Outgoing transport is provided by kinesin, and ingoing return traffic is provided by dynein. Dynein is minus-end directed. There are many forms of kinesis and dynein motor proteins, and each is thought to carry a different cargo. The studies on transport in the axon led to the naming of kinesin. In the nervous system, axons may be myelinated, or unmyelinated. This is the provision of an insulating layer, called a myelin sheath. In the peripheral nervous system axons are myelinated by glial cells known as Schwann cells. In the central nervous system the myelin sheath

pos: Schwann cell Schwann cells. Schwann cells are a variety of glial cells that keep peripheral nerve fibres (both myelinated and unmyelinated) alive. In myelinated axons, Schwann cells form the myelin sheath. The sheath is not continuous. Individual myelinating Schwann cells cover about 100 μm of an axon—equating to about 10,000 Schwann cells along a 1-m length of the axon. The gaps between adjacent Schwann cells are called nodes of Ranvier. 9-O-Acetyl GD3 ganglioside is an acetylated glycolipid which is found in the cell membranes of many types of vertebrate cells. During peripheral nerve regeneration, 9-O-acetyl GD3 is expressed by Schwann cells. The

pos: Axon system Schwann cells form the myelin sheath of a myelinated axon. In the central nervous system oligodendrocytes form the insulating myelin. Along myelinated nerve fibers, gaps in the myelin sheath known as nodes of Ranvier occur at evenly spaced intervals. The myelination enables an especially rapid mode of electrical impulse propagation called saltatory conduction. The myelinated axons from the cortical neurons form the bulk of the neural tissue called white matter in the brain. The myelin gives the white appearance to the tissue in contrast to the grey matter of the cerebral cortex which contains the neuronal cell bodies. A

pos: Wallerian degeneration axonal injury in both the peripheral nervous system (PNS) and central nervous system (CNS). It occurs in the section of the axon distal to the site of injury and usually begins within 24–36 hours of a lesion. Prior to degeneration, the distal section of the axon tends to remain electrically excitable. After injury, the axonal skeleton disintegrates, and the axonal membrane breaks apart. Axonal degeneration is followed by degradation of the myelin sheath and infiltration by macrophages. The macrophages, accompanied by Schwann cells, serve to clear the debris from the degeneration. Schwann cells respond to loss of axons by extrusion

pos: Axon is provided by another type of glial cell, the oligodendrocyte. Schwann cells myelinate a single axon. An oligodendrocyte can myelinate up to 50 axons. Nodes of Ranvier (also known as "myelin sheath gaps") are short unmyelinated segments of a myelinated axon, which are found periodically interspersed between segments of the myelin sheath. Therefore, at the point of the node of Ranvier, the axon is reduced in diameter. These nodes are areas where action potentials can be generated. In saltatory conduction, electrical currents produced at each node of Ranvier are conducted with little attenuation to the next node in line, where

pos: Charcot–Marie–Tooth disease exchange molecular signals that regulate survival and differentiation. These signals are disrupted in CMT. Demyelinating Schwann cells causes abnormal axon structure and function. They may cause axon degeneration, or they may simply cause axons to malfunction. The myelin sheath allows nerve cells to conduct signals faster. When the myelin sheath is damaged, nerve signals are slower, and this can be measured by a common neurological test, electromyography. When the axon is damaged, though, this results in a reduced compound muscle action potential. CMT can be diagnosed through symptoms, through measurement of the speed of nerve impulses (nerve conduction studies), through

pos: Site-specific recombinase technology a promoter results in localized, tissue-specific expression. As an example, Leone et al. have placed the transcription unit under the control of the regulatory sequences of the myelin proteolipid protein (PLP) gene, leading to induced removal of targeted gene sequences in oligodendrocytes and Schwann cells. The specific DNA fragment recognized by Cre remains intact in cells, which do not express the PLP gene; this in turn facilitates empirical observation of the localized effects of genome alterations in the myelin sheath that surround nerve fibers in the central nervous system (CNS) and the peripheral nervous system (PNS). Selective Cre expression has

pos: Wallerian degeneration PNS. Another factor that affects degradation rate is the diameter of the axon: larger axons require a longer time for the cytoskeleton to degrade and thus take a longer time to degenerate. Myelin is a phospholipid membrane that wraps around axons to provide them with insulation. It is produced by Schwann cells in the PNS, and by oligodendrocytes in the CNS. Myelin clearance is the next step in Wallerian degeneration following axonal degeneration. The cleaning up of myelin debris is different for PNS and CNS. PNS is much faster and efficient at clearing myelin debris in comparison to CNS, and

pos: Neurilemma Neurilemma Neurilemma (also known as neurolemma, sheath of Schwann, or Schwann's sheath) is the outermost nucleated cytoplasmic layer of Schwann cells (also called neurilemmocytes) that surrounds the axon of the neuron. It forms the outermost layer of the nerve fiber in the peripheral nervous system. The neurilemma is underlain by the myelin sheath (referred to as the medullary sheath in the included illustrations). In the central nervous system, axons are myelinated by oligodendrocytes, thus lack neurilemma. The myelin sheaths of Oligodendrocytes do not have neurilemma because excess cytoplasm is directed centrally toward the oligodendrocyte cell body. Neurilemma serves a protective

pos: Myelin protein zero Myelin protein zero Myelin protein zero (P0, MPZ) is a single membrane glycoprotein which in humans is encoded by the "MPZ" gene. P0 is a major structural component of the myelin sheath in the peripheral nervous system (PNS). Myelin protein zero is expressed by Schwann cells and accounts for over 50% of all proteins in the peripheral nervous system, making it the most common protein expressed in the PNS. Mutations in myelin protein zero can cause myelin deficiency and are associated with neuropathies like Charcot–Marie–Tooth disease and Dejerine–Sottas disease. In humans, the gene that encodes myelin protein zero is located

pos: Myelin recorded conduction speed (across both vertebrates and invertebrates) is found in the ensheathed axons of the Kuruma shrimp, an invertebrate, ranging between 90 and 200 m/s (cf 100–120 m/s for the fastest myelinated vertebrate axon.) Myelin Myelin is a lipid-rich (fatty) substance formed in the central nervous system (CNS) by glial cells called oligodendrocytes, and in the peripheral nervous system (PNS) by Schwann cells. Myelin insulates nerve cell axons to increase the speed at which information (encoded as an electrical signal) travels from one nerve cell body to another (as in the CNS) or, for example, from a nerve cell

pos: Myelin protein zero result in neuropathy because the cytoplasmic domain has been demonstrated to be necessary for homotypic interactions. Myelin protein zero Myelin protein zero (P0, MPZ) is a single membrane glycoprotein which in humans is encoded by the "MPZ" gene. P0 is a major structural component of the myelin sheath in the peripheral nervous system (PNS). Myelin protein zero is expressed by Schwann cells and accounts for over 50% of all proteins in the peripheral nervous system, making it the most common protein expressed in the PNS. Mutations in myelin protein zero can cause myelin deficiency and are associated with neuropathies like

pos: Myelin incisure continuous, but due to imperfect nature of the process by which Schwann cells wrap the nerve axon, this wrapping process can sometimes leave behind small pockets of residual cytoplasm displaced to the periphery during the formation of the myelin sheath. These pockets, or "incisures", can subdivide the myelinated axon into irregular portions. These staggered clefts also provide communication channels between layers by connecting the outer collar of cytoplasm of the Schwann cell to the deepest layer of myelin sheath. Primary incisures which appear ab initio in myelination and always extend across the whole radial thickness of the myelin sheath but

pos: Action potential by having a very high concentration of voltage-activated sodium channels. In general, it is considered to be the spike initiation zone for action potentials, i.e. the trigger zone. Multiple signals generated at the spines, and transmitted by the soma all converge here. Immediately after the axon hillock is the axon. This is a thin tubular protrusion traveling away from the soma. The axon is insulated by a myelin sheath. Myelin is composed of either Schwann cells (in the peripheral nervous system) or oligodendrocytes (in the central nervous system), both of which are types of glial cells. Although glial cells are

pos: Neurofibroma nervous system (PNS) axons with myelin, nonmyelinating Schwann cells encapsulate small diameter PNS axons with their cytoplasmic processes. Nonmyelinating Schwann cells are the neoplastic element in neurofibromas. This conglomeration of nonmyelinating Schwann cells and axons is called a Remak bundle. While nonmyelinating Schwann cells are the origin of neurofibromas, the mutations that make them susceptible to this transformation occur in Schwann cell precursors during early nerve development. Mutated nonmyelinating Schwann cells do not form normal Remak bundles. Instead, they fail to properly surround and segregate target axons. It is unknown at this time why, if both types of Schwann cells

pos: Peripheral myelin protein 22 Peripheral myelin protein 22 Growth arrest-specific protein 3 (GAS-3), also called peripheral myelin protein 22 (PMP22), is a protein which in humans is encoded by the "PMP22" gene. PMP22 is a 22 kDa transmembrane glycoprotein made up of 160 amino acids, and is mainly expressed in the Schwann cells of the peripheral nervous system. Schwann cells show high expression of PMP22, where it can constitute 2-5% of total protein content in compact myelin. Compact myelin is the bulk of the peripheral neuron's myelin sheath, a protective fatty layer that provides electrical insulation for the neuronal axon. The level of PMP22

pos: Schwann cell Schwann cell Schwann cells (named after physiologist Theodor Schwann) or neurolemmocytes are the principal glia of the peripheral nervous system (PNS). Glial cells function to support neurons and in the PNS, also include satellite cells, olfactory ensheathing cells, enteric glia and glia that reside at sensory nerve endings, such as the Pacinian corpuscle. The two types of Schwann cells are myelinating and nonmyelinating. Myelinating Schwann cells wrap around axons of motor and sensory neurons to form the myelin sheath. The Schwann cell promoter is present in the downstream region of the human dystrophin gene that gives shortened transcript that are

pos: Schwann cell increases speed of conduction and saves energy. Nonmyelinating Schwann cells are involved in maintenance of axons and are crucial for neuronal survival. Some group around smaller axons (External image here) and form Remak bundles. Myelinating Schwann cells begin to form the myelin sheath in mammals during fetal development and work by spiraling around the axon, sometimes with as many as 100 revolutions. A well-developed Schwann cell is shaped like a rolled-up sheet of paper, with layers of myelin between each coil. The inner layers of the wrapping, which are predominantly membrane material, form the myelin sheath, while the outermost layer

pos: Wallerian degeneration that fail to make contact to axon and receive axon signals undergo apoptosis. Experiments in Wallerian degeneration have shown that upon injury oligodendrocytes either undergo programmed cell death or enter a state of rest. Therefore, unlike Schwann cells, oligodendrocytes fail to clean up the myelin sheaths and their debris. In experiments conducted on rats myelin sheaths were found for up to 22 months. Therefore, CNS rates of myelin sheath clearance are very slow and could possibly be the cause for hindrance in the regeneration capabilities of the CNS axons as no growth factors are available to attract the proximal axons.

pos: Neurilemma function for peripheral nerve fibers. Damaged nerve fibers may regenerate if the cell body is not damaged and the neurilemma remains intact. The neurilemma forms a regeneration tube through which the growing axon re-establishes its original connection. A neurilemoma is a tumor of the neurilemma. Neurilemma Neurilemma (also known as neurolemma, sheath of Schwann, or Schwann's sheath) is the outermost nucleated cytoplasmic layer of Schwann cells (also called neurilemmocytes) that surrounds the axon of the neuron. It forms the outermost layer of the nerve fiber in the peripheral nervous system. The neurilemma is underlain by the myelin sheath (referred to

pos: Node of Ranvier the increase in length of the myelin sheath can be accounted solely by the increase in length of axon covered by each successive turn of the spiral, as previously explained. At the junction of two Schwann cells along an axon, the directions of the lamellar overhang of the myelin endings are of opposite sense. This junction, adjacent of the Schwann cells, constitutes the region designated as the node of Ranvier. Researchers prove that in the developing CNS, Nav1.2 is initially expressed at all forming nodes Ranvier. Upon maturation, nodal Nav1.3 is down-regulated and replaced by Nav1.6. Naz1.2 is also expressed

pos: Guillain–Barré syndrome syndrome is caused by an immune attack on the nerve cells of the peripheral nervous system and their support structures. The nerve cells have their body (the soma) in the spinal cord and a long projection (the axon) that carries electrical nerve impulses to the neuromuscular junction where the impulse is transferred to the muscle. Axons are wrapped in a sheath of Schwann cells that contain myelin. Between Schwann cells are gaps (nodes of Ranvier) where the axon is exposed. Different types of Guillain–Barré syndrome feature different types of immune attack. The demyelinating variant (AIDP, see below) features damage to

pos: Nerve allograft become more relevant. An axon is the part of a neuron which conducts electrical impulses. Axons are surrounded by myelin, which contain Schwann cells. Schwann cells improve the electrical conduction. The myelin is surrounded by endoneurium, which is a protective sheath of connective tissue. This is surrounded by perineurium and epineurium, of which the latter is the outmost layer of dense connective tissue. When it comes to nerve repair, it is crucial that those layers make a good connection. There are several kinds of organ transplantation techniques. The nervus suralis, a nerve from the lower leg, is most often used.

pos: Peripheral nerve injury classification It is a temporary interruption of conduction without loss of axonal continuity.In neurapraxia, there is a physiologic block of nerve conduction in the affected axons. Other characteristics: It involves loss of the relative continuity of the axon and its covering of myelin, but preservation of the connective tissue framework of the nerve ( the encapsulating tissue, the epineurium and perineurium, are preserved ). Other characteristics: It is a total severance or disruption of the entire nerve fiber.A peripheral nerve fiber contains an axon (Or long dendrite), myelin sheath (if existence), their schwann cells, and the endoneurium. Neurotmesis may be partial

pos: Schwann cell vertebrate nervous system relies on the myelin sheath for insulation and as a method of decreasing membrane capacitance in the axon. The action potential jumps from node to node, in a process called saltatory conduction, which can increase conduction velocity up to 10 times, without an increase in axonal diameter. In this sense, Schwann cells are the PNS's analogues of the central nervous system's oligodendrocytes. However, unlike oligodendrocytes, each myelinating Schwann cell provides insulation to only one axon (see image). This arrangement permits saltatory conduction of action potentials with repropagation at the nodes of Ranvier. In this way, myelination greatly

pos: Action potential Myelin is a multilamellar membrane that enwraps the axon in segments separated by intervals known as nodes of Ranvier. It is produced by specialized cells: Schwann cells exclusively in the peripheral nervous system, and oligodendrocytes exclusively in the central nervous system. Myelin sheath reduces membrane capacitance and increases membrane resistance in the inter-node intervals, thus allowing a fast, saltatory movement of action potentials from node to node. Myelination is found mainly in vertebrates, but an analogous system has been discovered in a few invertebrates, such as some species of shrimp. Not all neurons in vertebrates are myelinated; for example, axons

pos: Dock7 neurite which goes on to form the axon of the polarised neuron. In Schwann cells (which generate an insulating layer, known as the myelin sheath, around axons of the peripheral nervous system) Dock7 appears to be activated downstream of the neuregulin receptor ErbB2, which receives signals from the axon that induce Schwann cell proliferation, migration and myelination. ErbB2 has been shown to tyrosine phosphorylate Dock7 and thus promote Schwann cell migration. DOCK proteins are known activators of small G proteins of the Rho family. A study of Dock7 in HEK 293 cells and hippocampal neurons has shown that it can

pos: Node of Ranvier nodes and the degeneration and regeneration of cut fibers had a great influence on Parisian neurology at the Salpêtrière. Soon afterwards, he discovered gaps in sheaths of nerve fibers, which were later called the Nodes of Ranvier. This discovery later led Ranvier to careful histological examination of myelin sheaths and Schwann cells. Node of Ranvier Nodes of Ranvier ( , ), also known as myelin-sheath gaps, occur along a myelinated axon where the axolemma is exposed to the extracellular space. Nodes of Ranvier are uninsulated and highly enriched in ion channels, allowing them to participate in the exchange of ions

pos: Charcot–Marie–Tooth disease cells, the mitochondria travel down the long axons. In some forms of CMT, mutated "MFN2" causes the mitochondria to form large clusters, or clots, which are unable to travel down the axon towards the synapses. This prevents the synapses from functioning. CMT is divided into the primary demyelinating neuropathies (CMT1, CMT3, and CMT4) and the primary axonal neuropathies (CMT2), with frequent overlap. Another cell involved in CMT is the Schwann cell, which creates the myelin sheath, by wrapping its plasma membrane around the axon. Neurons, Schwann cells, and fibroblasts work together to create a functional nerve. Schwann cells and neurons

pos: Wallerian degeneration attributed to the ErbB2 receptors and the ErbB3 receptors. This proliferation could further enhance the myelin cleaning rates and plays an essential role in regeneration of axons observed in PNS. Schwann cells emit growth factors that attract new axonal sprouts growing from the proximal stump after complete degeneration of the injured distal stump. This leads to possible reinnervation of the target cell or organ. However, the reinnervation is not necessarily perfect, as possible misleading occurs during reinnervation of the proximal axons to target cells. In comparison to Schwann cells, oligodendrocytes require axon signals to survive. In their developmental stages, oligodendrocytes

pos: Oligodendrocyte (GDNF), brain-derived neurotrophic factor (BDNF), or insulin-like growth factor-1 (IGF-1). In addition, the nervous system of mammals depends crucially on myelin sheaths, which reduce ion leakage and decrease the capacitance of the cell membrane. Myelin also increases impulse speed, as saltatory propagation of action potentials occurs at the nodes of Ranvier in between Schwann cells (of the PNS) and oligodendrocytes (of the CNS). Furthermore, impulse speed of myelinated axons increases linearly with the axon diameter, whereas the impulse speed of unmyelinated cells increases only with the square root of the diameter. The insulation must be proportional to the diameter of

pos: Nerve Nerve A nerve is an enclosed, cable-like bundle of nerve fibres called axons, in the peripheral nervous system. A nerve provides a common pathway for the electrochemical nerve impulses called action potentials that are transmitted along each of the axons to peripheral organs or, in the case of sensory nerves, from the periphery back to the central nervous system. Each axon within the nerve is an extension of an individual neuron, along with other supportive cells such as Schwann cells that coat the axons in myelin. Within a nerve, each axon is surrounded by a layer of connective tissue called

pos: Endoneurium meshes. Similar structures occur around some nervous components elsewhere in the body, for example around the Schwann cells on the peripheral side of the transitional zone on the auditory nerve. Endoneurium The endoneurium (also called endoneurial channel, endoneurial sheath, endoneurial tube, or Henle's sheath) a layer of delicate connective tissue around the myelin sheath of each myelinated nerve fiber. Its component cells are called endoneurial cells. The endoneuria with their enclosed nerve fibers are bundled into groups called nerve fascicles, each fascicle within its own protective sheath called a perineurium. In sufficiently large nerves multiple fascicles, each with its blood

pos: Nerve injury before nerve regeneration and can be described as a cleaning or clearing process that essentially prepares the distal stump for reinnervation. Schwann cells are glial cells in the peripheral nervous system that support neurons by forming myelin that encases nerves. During Wallerian degeneration Schwann cells and macrophages interact to remove debris, specifically myelin and the damaged axon, from the distal injury site. (medscape) Calcium has a role in the degeneration of the damage axon. Bands of Büngner are formed when un-innervated Schwann cells proliferate and the remaining connective tissue basement membrane forms endoneurial tubes. Bands of Büngner are important for

pos: Cryoneurolysis tissue layer. These axons are bundled into fascicles surrounded by the perineurium connective tissue layer. Multiple fascicles are then surrounded by the epineurium, which is the outermost connective tissue layer of the nerve. The axons of myelinated nerves have a myelin sheath made up of Schwann cells that coat the axon. Classification of nerve damage was well-defined by Sir Herbert Seddon and Sunderland in a system that remains in use. The adjacent table details the forms (neurapraxia, axonotmesis and neurotmesis) and degrees of nerve injury that occur as a result of exposure to various temperatures. Cryoneurolysis treatments that use nitrous

pos: Intraocular schwannoma elimination of cellular debris, regeneration and upkeep of axons. Additionally, Schwann cells are actively involved in creating an inflammation reaction as a response to an injury of the PNS. Because injuries can lead to damaged axons, Schwann cells aid in fixing axonal damage and promoting new growth. Due to their healing properties, these cells can be used in spinal cord injuries to encourage regeneration of damaged axons. Finally, these multipurpose cells are key in the formation of protective outer barrier, or the perineurial sheath, that creates a vital separation for peripheral nerves. There are also several diseases linked to Schwann

pos: Myelinogenesis the process of regeneration, Schwann cells re-synthesize proteins associated with myelin-specific proteins when axonal presence is re-established. A key part of the experiment was to indicate that Schwann cells don't synthesize myelin-proteins in the absence of axons. Synthesis of detectable myelin-specific proteins did not occur in Schwann cells free of axons and thus proving that the axons instruct the Schwann cells to initiate the production of myelin proteins immediately after establishment of axonal association. Even though the axon completely controlled the synthesis of these proteins, the axon alone isn’t enough for myelinogenesis. As the experiment progressed, it became more evident

pos: Wallerian degeneration of myelin in CNS and PNS. Regeneration follows degeneration. Regeneration is rapid in PNS, allowing for rates of up to 1 millimeter a day of regrowth. Grafts may also be needed to allow for appropriate reinnervation. It is supported by Schwann cells through growth factors release. CNS regeneration is much slower, and is almost absent in most vertebrate species. The primary cause for this could be the delay in clearing up myelin debris. Myelin debris, present in CNS or PNS, contains several inhibitory factors. The prolonged presence of myelin debris in CNS could possibly hinder the regeneration. An experiment conducted

pos: Sulfatide structural component of the membrane. This is because sulfatide is upregulated, i.e.there is an increase in sulfatide, prior to the myelin sheath being wrapped around the axon, and experiments in cerebroside sulfotransferase (CST) deficient mice have shown that sulfatide operates as a negative regulator (inhibitor) of oligodendrocyte differentiation. Accordingly, further research has demonstrated that when sulfatide is deficient, there is a two to threefold increase in oligodendrocyte differentiation, evidence providing support that sulfatide operates as a negative regulator or inhibitor of oligodendrocyte differentiation. Myelination also appears to be stimulated by sulfatide in the Schwann Cells. Such stimulation is thought to

pos: Nerve injury are active in demylenation of injured nerves before macrophages are even present at the site of nerve injury. Electron microscopy and immunohistochemical staining analysis of teased nerve fibers shows that before macrophages arrive at the injury site, myelin is fragmented and myelin debris and lipid droplets are found in the cytoplasm of Schwann cells, indicating phagocytic activitiy before macrophages arrive. Schwann cell activity includes recruitment of macrophages to the injury site. Monocyte chemoattractant protein (MCP-1) plays a role in recruiting monocytes/macrophages. In tellurium-induced demylenation with no axon degeneration, nerve crush with axon degeneration, and nerve transection with axon degeneration an

pos: Peripheral myelin protein 22 heterophilic interaction between PMP22 protein and Myelin protein zero (MPZ). Although the PMP22 mechanism of action in myelinating Schwann cells is not fully known, it plays an essential role in the formation and maintenance of compact myelin. When Schwann cells come into contact with a neuronal axon, expression of PMP22 is significantly up-regulated, whereas PMP22 is down-regulated during axonal degeneration or transection. PMP22 has shown association with zonula-occludens 1 and occludin, proteins that are involved in adhesion with other cells and the extracellular matrix, and also support functioning of myelin. Along with cell adhesion function, PMP22 is also up-regulated during

pos: Nerve tissue protein Nerve tissue protein Nerve tissue is a biological molecule related to the function and maintenance of normal nervous tissue. An example would include, for example, the generation of myelin which insulates and protects nerves. These are typically calcium-binding proteins. There are two types of myelin the first is ogliodendrocyte- Myelin which can be found in the mammalian Central Nervous System (CNS) and the second is Schwann cells which are found in the Peripheral Nervous System (PNS). Myelination of axons by these Schwann cells are essential for normal nerve function. Peripheral nerves rely on communication between axons and Schwaan cells. Prion

pos: SH3TC2 and to the perinuclear endocytic recycling compartment. Mice lacking Sh3tc2 have an abnormal organization of the node of Ranvier consistent with the idea that the protein might have a role in myelination or in axon – glial cell interactions. Mutations in this gene result in autosomal recessive Charcot-Marie-Tooth disease type 4C, a childhood-onset neurodegenerative disease characterized by demyelination of motor and sensory neurons. SH3TC2 SH3 domain and tetratricopeptide repeats-containing protein 2 is a protein that in humans is encoded by the "SH3TC2" gene. It is believed to be expressed in the Schwann cells that wrap the myelin sheath around nerves.

pos: Myelin large proportion of axons are unmyelinated. Instead, they are ensheathed by non-myelinating Schwann cells known as Remak SCs and arranged in Remak bundles. In the CNS, non-myelinated (or intermittently myelinated axons; meaning having long non-myelinated regions between myelinated segments), intermingle with myelinated ones and are entwined, at least partially, by the processes of another type of glial cell called the astrocyte. CNS myelin differs slightly in composition and configuration from PNS myelin, but both perform the same "insulating" function (see above). Being rich in lipid, myelin appears white; hence, the name given to the "white matter" of the CNS. Both

pos: Nervous tissue PNS are satellite cells and Schwann cells. In the central nervous system (CNS), the tissue types found are grey matter and white matter. The tissue is categorized by its neuronal and neuroglial components. Neurons are cells with specialized features that allow them to receive and facilitate nerve impulses, or action potentials, across their membrane to the next neuron. They possess a large cell body (soma), with cell projections called dendrites and an axon. Dendrites are thin, branching projections that receive electrochemical signaling (neurotransmitters) to create a change in voltage in the cell. Axons are long projections that carry the action

pos: Alpha motor neuron signals as action potentials, rapid changes in electrical activity that propagate from the cell body to the end of the axon. To increase the speed at which action potentials travel, α-MN axons have large diameters and are heavily myelinated by both oligodendrocytes and Schwann cells. Oligodendrocytes myelinate the part of the α-MN axon that lies in the central nervous system (CNS), while Schwann cells myelinate the part that lies in the peripheral nervous system (PNS). The transition between the CNS and PNS occurs at the level of the pia mater, the innermost and most delicate layer of meningeal tissue surrounding

pos: Schwann cell myelin. It has been shown to control a set of genes responsible for interfering with this feature in the axon changing it from a pro-myelinating to myelinating state. In this way, in Krox-20 double knock out mice, it has been recorded that hindbrain segmentation is affected as well as myelination of Schwann cell associated axons. Indeed, in these mice, the Schwann cells are not able to perform their myelination properly as they only wrap their cytoplasmic processes one and half turn around the axon and despite the fact that they still express the early myelin marker, late myelin gene products

pos: Vestibular schwannoma Vestibular schwannoma A vestibular schwannoma (VS) is a benign primary intracranial tumor of the myelin-forming cells of the vestibulocochlear nerve (8th cranial nerve). A type of schwannoma, this tumor arises from the Schwann cells responsible for the myelin sheath that helps keep peripheral nerves insulated. Although it is also called an acoustic neuroma, this a misnomer for two reasons. First, the tumor usually arises from the vestibular division of the vestibulocochlear nerve, rather than the cochlear division. Second, it is derived from the Schwann cells of the associated nerve, rather than the actual neurons (neuromas). Approximately 2,000 to 3,000 cases

pos: Oligodendrocyte matter, typically in immunocompromised patients. Tumors of oligodendroglia are called oligodendrogliomas. The chemotherapy agent Fluorouracil (5-FU) causes damage to the oligodendrocytes in mice, leading to both acute central nervous system (CNS) damage and progressively worsening delayed degeneration of the CNS. Oligodendrocyte Oligodendrocytes (), or oligodendroglia, are a type of neuroglia discovered by Pío del Río Hortega. Their main functions are to provide support and insulation to axons in the central nervous system of some vertebrates, equivalent to the function performed by Schwann cells in the peripheral nervous system. Oligodendrocytes do this by creating the myelin sheath, which is 80% lipid

pos: Anti-MAG peripheral neuropathy around the axons that they serve. Damage to these cells result in degeneration of the myelin sheath and inevitably lead to problems in communication for the nervous system. Myelin-associated glycoprotein (MAG) is a glycoprotein that is specific to Schwann cells, which create myelin for nerve cells in the peripheral nervous system. Research through cloning of the rat MAG gene has shown that it is a type I transmembrane protein meaning that it contains domains both inside the cell membrane and outside the cell membrane. Expression of this glycoprotein is very specific to myelin-forming cells and begins very early in the

pos: Anti-MAG peripheral neuropathy to travel at a much faster rate, about fifteen times faster in certain cases. This ability allows the nervous system to send messages faster and more accurately. Disruption of the myelin sheath on cells that are normally myelinated allows leakage of action potential much like a faulty wire will allow leakage of electricity in a circuit. This slows the messages being sent along those nerves and disrupts normal function. Schwann cells are the cells in the peripheral nervous system that create and maintain myelin sheaths on neurons. These are the glial cells of the peripheral nervous system and are located

pos: Wallerian degeneration the third week after injury. While Schwann cells mediate the initial stage of myelin debris clean up, macrophages come in to finish the job. Macrophages are facilitated by opsonins, which label debris for removal. The 3 major groups found in serum include complement, pentraxins, and antibodies. However, only complement has shown to help in myelin debris phagocytosis. Murinson et al. (2005) observed that non-myelinated or myelinated Schwann cells in contact with an injured axon enter cell cycle thus leading to proliferation. Observed time duration for Schwann cell divisions were approximately 3 days after injury. Possible sources of proliferation signal are

neg: Neuroregeneration Neuroregeneration Neuroregeneration refers to the regrowth or repair of nervous tissues, cells or cell products. Such mechanisms may include generation of new neurons, glia, axons, myelin, or synapses. Neuroregeneration differs between the peripheral nervous system (PNS) and the central nervous system (CNS) by the functional mechanisms and especially the extent and speed. When an axon is damaged, the distal segment undergoes Wallerian degeneration, losing its myelin sheath. The proximal segment can either die by apoptosis or undergo the chromatolytic reaction, which is an attempt at repair. In the CNS, synaptic stripping occurs as glial foot processes invade the dead synapse.

neg: Myelin myelin does not form a single long sheath over the entire length of the axon. Rather, each myelin sheath insulates the axon over a single section and, in general, each axon comprises multiple long myelinated sections separated from each other by short gaps. Each myelin sheath is formed by the concentric wrapping of an oligodendrocyte or Schwann cell process around the axon. More precisely, myelin speeds the transmission of electrical impulses called action potentials along myelinated axons by insulating the axon and reducing axonal membrane capacitance. This results in saltatory conduction whereby the action potential "jumps" from one node of

neg: Charcot–Marie–Tooth disease complex regional pain syndrome, among other diseases. Charcot–Marie–Tooth disease is caused by mutations that cause defects in neuronal proteins. Nerve signals are conducted by an axon with a myelin sheath wrapped around it. Most mutations in CMT affect the myelin sheath, but some affect the axon. The most common cause of CMT (70–80% of the cases) is the duplication of a large region on the short arm of chromosome 17 that includes the gene "PMP22". Some mutations affect the gene "MFN2", which codes for a mitochondrial protein. Cells contain separate sets of genes in their nuclei and mitochondria. In nerve

neg: Node of Ranvier internodes under the compact myelin sheath, but are very similar in CNS and PNS. The axon is exposed to the extra-cellular environment at the node and is constricted in its diameter. The decreased axon size reflects a higher packing density of neurofilaments in this region, which are less heavily phosphorylated and are transported more slowly. Vesicles and other organelles are also increased at the nodes, which suggest that there is a bottleneck of axonal transport in both directions as well as local axonal-glial signaling. When a longitudinal section is made through a myelinating Schwann cell at the node, three distinctive

neg: Myelin regions such as the cerebral cortex, throughout life. Myelin is considered a defining characteristic of the jawed vertebrates (gnathostomes), but axons are ensheathed by glial cells in invertebrates, although these glial-wraps are quite different from vertebrate compact myelin, formed, as indicated above, by concentric wrapping of the myelinating cell process multiple times around the axon. Myelin was first described in 1854 by Rudolf Virchow, although it was over a century later, following the development of electron microscopy, that its glial cell origin and its ultrastructure became apparent. In vertebrates, not all axons are myelinated. For example, in the PNS, a

neg: Remyelination always be less than 1, but remyelinated axons tend to have values closer to 1, indicating a thinner myelin sheath than those myelinated naturally. The g-ratio differences are less apparent on smaller axons. The thinner myelin not only restores protection of the axon from degradation, but also restores a faster conduction velocity. The conduction velocity, however, is not as strong as naturally myelinated axons and the Nodes of Ranvier are inclined to be wider which results in less coverage in the axon by myelin than what is natural. Oligodendrocyte Precursor Cells, or OPC's, are the main cell responsible for the

neg: Myelin Ranvier, over a long myelinated stretch of the axon called the internode, before "recharging" at the next node of Ranvier, and so on, until it reaches the axon terminal. Nodes of Ranvier are the short (~1 micron) unmyelinated regions of the axon between adjacent long (~0.2 mm - >1 mm) myelinated internodes. Once it reaches the axon terminal, this electrical signal provokes the release of a chemical message or neurotransmitter that binds to receptors on the adjacent post-synaptic cell (e.g. nerve cell in the CNS or muscle cell in the PNS) at specialised regions called synapses. This "insulating" role for

neg: Myelin Protein content includes myelin basic protein (MBP), which is abundant in the CNS where it plays a critical, non-redundant role in formation of compact myelin; myelin oligodendrocyte glycoprotein (MOG), which is specific to the CNS; and proteolipid protein (PLP,) which is the most abundant protein in CNS myelin, but only a minor component of PNS myelin. In the PNS, myelin protein zero (MPZ or P0) has a similar role to that of PLP in the CNS in that it is involved in holding together the multiple concentric layers of glial cell membrane that constitute the myelin sheath. The primary lipid

neg: Neurapraxia opposed to the distal site. Neurapraxia occurs in the peripheral nervous system typically in the ulnar, median, and radial nerves of the upper body and in the sciatic and peroneal nerves of the lower body. Peripheral nerves are myelinated, relatively large, spatially complex cells whose size and connectivity typically make them more susceptible to damage and compromise their capacity to self-repair, although this is not the case in neurapraxia. Microscopic evidence has shown that there is damage to the myelin sheath, but not to the axon. Therefore, distal nerve fibers do not degenerate and the myelin damage can be repaired.

neg: Remyelination the inhibition and promotion factors of this physiological process. One way this process can be traced is by following different protein activation sequences which have shown just how quickly remyelination begins after injury (within a few of days). The most notable evidence that remyelination has taken place on an axon is its thin myelin sheath created by an oligodendrocyte, though the reason why the new myelin sheath is thinner remains unclear. This can be quantified in the g-ratio, the ratio between the diameter of the axon itself to the outer diameter of the myelinated fiber. So then, this value will

neg: CNS demyelinating autoimmune diseases insulation helps the axon of a nerve cell with the conduction and speed of the signal along the axon. CNS demyelination autoimmune disease causes the myelin sheath to deteriorate since the sense of recognition of self is lost.The loss of the myelin insulation either disrupts or prevents neural conduction along the nerve cell’s axon. Since the neural impulse is inhibited it may lead to paresthesia, muscle weakness, unsteady gait, paralysis, vision loss and other motor dysfunctions. The pathogenesis of the demyelination can vary. Some of the factors that contribute to the deteriorating of the myelin are due to inflammatory processes,

neg: Glia the CNS. These dendrocytes resemble an octopus bulbous body and contain up to fifteen arm-like processes. Each “arm” reaches out to a nerve fiber and spirals around it, creating a myelin sheath. This myelin sheath insulates the nerve fiber from the extracellular fluid as well as speeds up the signal conduction in the nerve fiber. Recent research indicates that glial cells of the hippocampus and cerebellum participate in synaptic transmission, regulate the clearance of neurotransmitters from the synaptic cleft, and release gliotransmitters such as ATP, which modulate synaptic function. Astrocytes are crucial in clearance of neurotransmitters from within the synaptic

neg: Neuron thin axon covered by the myelin sheath. Around the cell body is a branching dendritic tree that receives signals from other neurons. The end of the axon has branching terminals (axon terminal) that release neurotransmitters into a gap called the synaptic cleft between the terminals and the dendrites of the next neuron. Most neurons can be anatomically characterized as: Furthermore, some unique neuronal types can be identified according to their location in the nervous system and distinct shape. Some examples are: Afferent and efferent also refer generally to neurons that, respectively, bring information to or send information from the brain.

neg: Nervous tissue of different types of nerve cells, all of which have an axon. An axon is the long stem-like part of the cell that sends action potential signals to the next cell. Bundles of axons make up the nerves in the PNS and tracts in the CNS. Functions of the nervous system are sensory input, integration, control of muscles and glands, homeostasis, and mental activity. Nervous tissue is composed of neurons, also called nerve cells, and neuroglial cells. Four types of neuroglia found in the CNS are astrocytes, microglial cells, ependymal cells and oligodendrocytes. Two types of neuroglia found in the

neg: Axon the initial segment, the rest of the axon, and the axon telodendria, and axon terminals. It also includes the myelin sheath. The Nissl bodies that produce the neuronal proteins are absent in the axonal region. Proteins needed for the growth of the axon, and the removal of waste materials, need a framework for transport. This axonal transport is provided for in the axoplasm. The axon hillock is the area formed from the cell body of the neuron as it extends to become the axon. It precedes the initial segment. The received action potentials that are summed in the neuron are

neg: Endoneurium Endoneurium The endoneurium (also called endoneurial channel, endoneurial sheath, endoneurial tube, or Henle's sheath) a layer of delicate connective tissue around the myelin sheath of each myelinated nerve fiber. Its component cells are called endoneurial cells. The endoneuria with their enclosed nerve fibers are bundled into groups called nerve fascicles, each fascicle within its own protective sheath called a perineurium. In sufficiently large nerves multiple fascicles, each with its blood supply and fatty tissue, may be bundled within yet another sheath, the epineurium. The endoneurium contains a liquid known as endoneurial fluid, which contains little protein. In the peripheral nervous

neg: Nerve biopsy can help to determine the cause of such symptoms. The procedure is usually only performed when all other options have failed in determining the cause of a disease. It is an outpatient procedure that is performed under local anesthetic. A nerve biopsy can potentially find the cause of the numbness and/or pain experienced in the limbs. It can reveal if these symptoms are caused by damage to the myelin sheath, damage to the small nerves, destruction of the axon in the nerve cells or neuropathies. A sample piece of a nerve is cut from an affected area. The three different

neg: Tractography be many things: cell membranes, axons, myelin, etc.; but in white matter the principal barrier is the myelin sheath of axons. Bundles of axons provide a barrier to perpendicular diffusion and a path for parallel diffusion along the orientation of the fibers. Anisotropic diffusion is expected to be increased in areas of high mature axonal order. Conditions where the myelin or the structure of the axon are disrupted, such as trauma, tumors, and inflammation reduce anisotropy, as the barriers are affected by destruction or disorganization. Anisotropy is measured in several ways. One way is by a ratio called fractional anisotropy

neg: Perineurium lamellar arrangement consisting of one to several concentric layers. The perineurium is composed of perineurial cells, which are epithelioid myofibroblasts. Perineurial cells are sometimes referred to as myoepithelioid due to their epithelioid and myofibroblastoid properties including tight junctions, gap junctions, external laminae and contractility. The perineurium is a smooth, transparent tubular membrane which may be easily separated from the fibers it encloses. In contrast, the epineurium is a tough and mechanically resistant tissue which is not easily penetrated by a needle. Perineurium In the peripheral nervous system, the myelin sheath of each axon in a nerve is wrapped in a

neg: Brain is widely believed that activity-dependent modification of synapses is the brain's primary mechanism for learning and memory. Most of the space in the brain is taken up by axons, which are often bundled together in what are called "nerve fiber tracts". A myelinated axon is wrapped in a fatty insulating sheath of myelin, which serves to greatly increase the speed of signal propagation. (There are also unmyelinated axons). Myelin is white, making parts of the brain filled exclusively with nerve fibers appear as light-colored white matter, in contrast to the darker-colored grey matter that marks areas with high densities of

neg: Metachromatic leukodystrophy 5~20% of normal controls does not cause MLD. Without this enzyme, sulfatides build up in many tissues of the body, eventually destroying the myelin sheath of the nervous system. The myelin sheath is a fatty covering that protects nerve fibers. Without it, the nerves in the brain (central nervous system – CNS) and the peripheral nerves (peripheral nervous system – PNS) which control, among other things the muscles related to mobility, cease to function properly. Arylsulfatase A is activated by saposin B (Sap B), a non-enzymatic proteinaceous cofactor. When the arylsulfatase A enzyme level is normal but the sulfatides are

neg: Myelin structures and organelles such as mitochondria, along the axon. Recently, evidence came to light to support a role for the myelinating cell in "feeding" the axon. In other words, the myelinating cell seems to act as a local "fueling station" for the axon, which uses a great deal of energy to restore the normal balance of ions between it and its environment (see above and ), following the generation of action potentials. When a peripheral fiber is severed, the myelin sheath provides a track along which regrowth can occur. However, the myelin layer does not ensure a perfect regeneration of

neg: Remyelination Remyelination Remyelination is the process of propagating oligodendrocyte precursor cells to form oligodendrocytes to create new myelin sheaths on demyelinated axons in the CNS. This is a process naturally regulated in the body and tends to be very efficient in a healthy CNS. The process creates a thinner myelin sheath than normal, but it helps to protect the axon from further damage, from overall degeneration, and proves to increase conductance once again. Demyelinating diseases, such as multiple sclerosis, have been of utmost interest within the last couple of decades. Recent research is uncovering some of the many unknown pathways involved

neg: Polyneuropathy or by "classes" of polyneuropathy, in terms of which part of the nerve cell is affected mainly: the axon, the myelin sheath, or the cell body. Among the signs/symptoms of polyneuropathy, which can be divided (into sensory and hereditary) and are consistent with the following: The causes of polyneuropathy can be divided into hereditary and acquired and are therefore as follows: In regards to the pathophysiology of polyneuropathy, of course, the former depends on "which" polyneuropathy. For instance in the case of chronic inflammatory demyelinating polyneuropathy, one finds that it is a autoimmune disease. Here, T cells involvement has been

neg: CNS demyelinating autoimmune diseases CNS demyelinating autoimmune diseases CNS demyelinating autoimmune diseases are autoimmune diseases which primarily affect the central nervous system. Examples include: The brain and the spinal cord are the essential components of the central nervous system and it is responsible for the integration of the signals received from the afferent nerves and initiates action. The nerve cells, known as neurons, carry impulses throughout the body and the nerve impulses are carried along the axon. These microscopic nerve fibers, where the action potential occurs, are protected by a white, fatty tissue that surrounds and insulates it, known as the myelin sheath. This

neg: Sam Schmidt Paralysis Foundation produce a fatty substance called myelin, which wraps around axons in layers. Axon fibers insulated by myelin can carry electrical messages (also called action potentials) at a speed of 100 meters per second, while fibers without myelin can carry messages at a speed of only one meter per second. A spinal cord injury can compromise or destroy myelin. Messages are passed from neuron to neuron through synapses, small gaps between the cells, with the help of chemicals called neurotransmitters. To transmit a message across a synapse, neurotransmitter molecules are released from one neuron (the "pre-synaptic" neuron) and cross the gap

neg: Node of Ranvier smoothly, as they do in axons that lack a myelin sheath. The clustering of voltage-gated sodium and potassium ion channels at the nodes permits this behavior. Since an axon can be unmyelinated or myelinated, the action potential has two methods to travel down the axon. These methods are referred to as continuous conduction for unmyelinated axons, and saltatory conduction for myelinated axons. Saltatory conduction is defined as an action potential moving in discrete jumps down a myelinated axon. This process is outlined as the charge passively spreading to the next node of Ranvier to depolarize it to threshold which will

neg: Opicinumab is designed to prevent the advancement of demyelination associated with neurodegenerative disorders, specifically MS. It is believed to function by allowing young cells, which would normally be prevented from maturing by the LINGO-1 protein, to mature into functional oligodendrocytes. Oligodendrocytes support nerve axons and serve to maintain the myelin sheath that allows for the effective conduction of axon potentials. LINGO-1 is only found in the Central Nervous System (CNS) and is thought to be at least a partial causative agent of MS, an autoimmune disorder. It is thought that by allowing oligodendrocytes to mature, further disability advancement caused by MS

neg: Axon hillock the resting potential, and during which no action potential can begin (undershoot phase/refractory period). This undershoot phase ensures that the action potential propagates down the axon and not back up it. Once this initial action potential is initiated, principally at the axon hillock, it propagates down the length of the axon. Under normal conditions, the action potential would attenuate very quickly due to the porous nature of the cell membrane. To ensure faster and more efficient propagation of action potentials, the axon is myelinated. Myelin, a derivative of cholesterol, acts as an insulating sheath and ensures that the signal cannot

neg: Neuroregeneration previously created antibodies (passive immunisation). These strategies appear promising on animal models with experimental autoimmune encephalomyelitis (EAE), a model of MS. Monoclonal antibodies have also been used against inhibitory factors such as NI-35 and NOGO. Neuroregeneration Neuroregeneration refers to the regrowth or repair of nervous tissues, cells or cell products. Such mechanisms may include generation of new neurons, glia, axons, myelin, or synapses. Neuroregeneration differs between the peripheral nervous system (PNS) and the central nervous system (CNS) by the functional mechanisms and especially the extent and speed. When an axon is damaged, the distal segment undergoes Wallerian degeneration, losing its

neg: Neuralgia regenerate properly, the neuron loses its function or may not function properly. Neuron trauma is not an isolated event and may cause degenerative changes in surrounding neurons. When one or more neurons lose their function or begin to malfunction, abnormal signals sent to the brain may be translated as painful signals. Neuronal injury in the central nervous system (CNS) typically leads to local degeneration of the nerve axon and myelin sheath. Axonal debris in the CNS is eliminated by macrophages. Trauma to neurons in the CNS also causes a proliferation of glial cells that form a glial scar. Development of

neg: Cryoneurolysis oxide (boiling point of -88.5 °C) as the coolant fall in the range of an axonotmesis injury, or 2nd degree injury, according to the Sunderland classification system. Treatments of the nerve in this temperature range are reversible. Nerves treated in this temperature range experience a disruption of the axon, with Wallerian degeneration occurring distal to the site of injury. The axon and myelin sheath are affected, but all of the connective tissues (endoneurium, perineurium, and epineurium) remain intact. Following Wallerian degeneration, the axon regenerates along the original nerve path at a rate of approximately 1–2 mm per day. Cryoneurolysis differs

neg: Myelin ions back into the axon to restore the balance of ions between the intracellular (inside the cell i.e. axon in this case) and extracellular (outwith the cell) fluids. Whilst the role of myelin as an "axonal insulator" is well-established, other functions of myelinating cells are less well known or only recently established. The myelinating cell "sculpts" the underlying axon by promoting the phosphorylation of neurofilaments, thus increasing the diameter or thickness of the axon at the internodal regions; helps cluster molecules on the axolemma (such as voltage-gated sodium channels) at the node of Ranvier; and modulates the transport of cytoskeletal

neg: Guillain–Barré syndrome the myelin sheath by white blood cells (T lymphocytes and macrophages); this process is preceded by activation of a group of blood proteins known as complement. In contrast, the axonal variant is mediated by IgG antibodies and complement against the cell membrane covering the axon without direct lymphocyte involvement. Various antibodies directed at nerve cells have been reported in Guillain–Barré syndrome. In the axonal subtype, these antibodies have been shown to bind to gangliosides, a group of substances found in peripheral nerves. A ganglioside is a molecule consisting of ceramide bound to a small group of hexose-type sugars and containing

neg: Perineurium Perineurium In the peripheral nervous system, the myelin sheath of each axon in a nerve is wrapped in a delicate protective sheath known as the endoneurium. Within the nerve, axons targeting the same anatomical location are bundled together into groups known as fascicles, each surrounded by another protective sheath known as the perineurium. Several fascicles may be in turn bundled together with a blood supply and fatty tissue within yet another sheath, the epineurium. This grouping structure is analogous to the muscular organization system of epimysium, perimysium and endomysium. The perineurium is composed of connective tissue, which has a distinctly

neg: Motor nerve nerves, each axon is wrapped by the endoneurium, which is a layer of connective tissue that surrounds the myelin sheath. Bundles of axons are called fascicles, which are wrapped in perineurium. All of the fascicles wrapped in the perineurium are wound together and wrapped by a final layer of connective tissue known as the epineurium. These protective tissues defend nerves from injury, pathogens and help to maintain nerve function. Layers of connective tissue maintain the rate at which nerves conduct action potentials. Most motor pathways originate in the motor cortex of the brain. Signals run down the brainstem and spinal

neg: Myelin called oligodendrocyte precursor cells (OPCs; the precursors of oligodendrocytes) synthesise myelin, and in so doing, transform into mature myelinating oligodendrocytes. In humans, myelination begins early in the 3rd trimester, although only little myelin is present in either the CNS or the PNS at the time of birth. During infancy, myelination progresses rapidly, with increasing numbers of axons acquiring myelin sheaths. This corresponds with the development of cognitive and motor skills, including language comprehension, speech acquisition, crawling and walking. Myelination continues through adolescence and early adulthood and although largely complete at this time, myelin sheaths can be added in grey matter

neg: Mesaxon connection of the outer cell membrane to the compact myelin sheath. The inner mesaxon (Terminologia histologica: Mesaxon internum) is the connection between the myelin sheath and the inner part of the cell membrane of the Schwann cell which is directly opposite the axolemma, i.e. the cell membrane of the nerve fibre ensheathed by the Schwann cell. Mesaxon In neurobiology, a mesaxon is a pair of parallel plasma membranes of a Schwann cell, marking the point of edge-to-edge contact by the Schwann cell encircling the axon. A single Schwann cell of the peripheral nervous system will wrap around and support only

neg: Pathology of multiple sclerosis the reasons why, especially in early phases of the disease, symptoms tend to decrease or disappear temporarily. Nevertheless, nerve damage and irreversible loss of neurons occur early in MS. The oligodendrocytes that originally formed a myelin sheath cannot completely rebuild a destroyed myelin sheath. However, the central nervous system can recruit oligodendrocyte stem cells capable of proliferation and migration and differentiation into mature myelinating oligodendrocytes. The newly formed myelin sheaths are thinner and often not as effective as the original ones. Repeated attacks lead to successively fewer effective remyelinations, until a scar-like plaque is built up around the damaged axons.

neg: Pioneer axon growing from guidepost to guidepost cells. In addition, pioneer axons can act as guidepost cells to more distant pioneer neurons. Studies that involved selective destruction of guidepost cells resulted in pioneer axons becoming unable to navigate normally to the CNS from the PNS. Instead, the pioneer axons assumed alternate configurations and followed different trajectories. In addition, without the guidepost cells, the pioneer axons did not find the stereotyped route that pioneer axons would normally navigate. It has been shown that glial cells also play a role in axon guidance in various ways. In particular, glial cells demonstrate an interaction with

neg: Vitamin D and neurology lack of "Nurr1" expression leads to impaired DA neuronal development. Failure to form DA neurons would lead to lower dopamine concentrations in the basal ganglia. Additionally, rats lacking "Nurr1" exhibited hypoactivity followed by death shortly after birth. Multiple sclerosis (MS) is an autoimmune disease causing demyelination within the central nervous system. In the central nervous system, there are many cells encased in a fatty coating called the myelin sheath. This sheath allows for informational signals to be transmitted at greater speeds down through the cell. In multiple sclerosis, this sheath deterioration causes a slower transmission of nerve signals. This ultimately

neg: Saltatory conduction Although the action potential appears to jump along the axon, this phenomenon is actually just the rapid, almost instantaneous, conduction of the signal inside the myelinated portion of the axon. In addition to increasing the speed of the nerve impulse, the myelin sheath helps in reducing energy expenditure over the axon membrane as a whole, because the amount of sodium and potassium ions that need to be pumped to bring the concentrations back to the resting state following each action potential is decreased. Saltatory conduction occurs widely in the myelinated nerve fibers of vertebrates, but was later discovered in a