A nerve cell or neuron usually consists of the cell body, of the cell body near short processes (dendrites) and of a neurite, which can reach in humans a length of over one meter. While the dendrites are usually not covered, most neurites are protected by a myelin or medullary sheath and then called an axon.
Typically, the myelin sheath is interrupted every 0.2 to 1.5 millimeters in length by a so-called Ranvier's Schnürring, so that the appearance of the axon somewhat reminiscent of a string of pearls with a string of elongated beads. The myelin sheaths isolate the nerve process electrically and not only provide protection, but also allow a much higher speed in the transmission of nerve stimuli by so-called saltatory stimulus transmission, which "jumps" from lacing ring to lacing ring.
The superstructure of myelin sheaths consists mainly of lipids such as cholesterol and phospholipids as well as of special structural proteins. The structure and composition of myelin sheaths is somewhat reminiscent of plasmalemm, the cell membrane of human and animal cells.
The medullary sheaths of the axons of the peripheral nervous system (PNS) are formed by Schwann cells and those of the central nervous system (CNS) by oligodendrocytes. Both types of cells belong to the glial cells, which take over support functions for the neurons and how the nerve cells themselves derive from the ectoderm.
Schwann cells spirally wrap each section of an axon in a spiral with a myelin layer, whose exact composition is similar to that of its plasmalemembrane, its cell membrane. For example, axons may well be wrapped with up to 50 double layers of the cell membrane. In the CNS, outgrowths grow out of the soma of the oligodendrocytes, making contact with the axons and enveloping them with a myelin sheath. A dendrocyte can simultaneously "wrap" axon sections of several axons.
The regular interruptions of the medullary sheaths in the form of Ranvier's Schnürringe at a distance of 0.2 to 1.5 millimeters play an important role in the transmission of stimuli. The Ranvier lacing rings leave very narrow spaces of about one micron each free, at which the nerve tracts are practically bare without electrical insulation.
The myelin sheaths of the axons perform several functions, which in detail are all important for the interaction of the nervous system and justify its functionality. The medullary sheath offers mechanical protection to the internal neurite and at the same time electrical isolation, which is interrupted only at the Ranvier's lacing rings.
The regular interruptions of isolation are crucial to the speed and nature of the transmission of action potentials. At rest, the axon inside has the so-called resting potential, which is characterized by an excess of negatively charged proteins and positively charged potassium ions over an excess of negatively charged chloride and positively charged sodium ions in the extracellular space outside the plasma membrane of the axon. The slightly negative resting potential (membrane potential) is maintained by ion channels and actively controllable sodium-potassium pumps in the membrane.
If the nerve cell receives a certain stimulus, it is depolarized, the electrical conditions are reversed at short notice, and the action potential arises via voltage-controlled sodium and potassium ion channels, which, however, only last about 0.1 to 0.2 milliseconds. The action potential in the axon depolarizes the next lacing ring and builds up an action potential.
This means that the relatively slow and cumbersome forwarding of stimuli is bridged by continuous transmission of the action potential and is replaced by the erratic (saltatory) impulse transmission from lacing ring to lacing ring. The "nerve speed" thereby increases from about 1 to 2 m / sec in neurites without a medullary sheath up to 120 m / sec in axons with thick medullary sheath. Another task of myelin sheath is the supply of the nerves.
The most important diseases and conditions directly related to myelin sheaths are diseases that lead to the breakdown and demyelination of the nerves. The demyelination of the axons - as the demyelination is also called - are based either on genetic defects known as triggers of hereditary motor-sensitive neuropathies or, for example, on the autoimmune disease multiple sclerosis (MS).
Other causes such as excessive chronic alcohol consumption, diabetic neuropathy, Lyme disease or myelin breakdown as an undesirable side effect of drugs come as a cause in question. Hereditary motor-sensitive neuropathies manifest themselves by gradual degradation of the myelin sheaths or there are problems with the structure or synthesis of the medullary sheaths from the outset. The genetic disease Morbus Krabbe is a special situation because it does not lead to a breakdown of myelin, but to an accumulation of harmful degradation products from the myelin metabolism due to lack of enzymes.
A demyelinization of axons can also be done by toxic agents or often suffer from a lack of certain B vitamins such as B6 and B12, among the alcoholic. The autoimmune disease MS, whose causes are (still) not fully understood, is relatively common in Central Europe and affects about twice as many women as men. The chronic inflammatory disease of the CNS leads to multiple or multiple (multiple) zones in the white matter that are affected by demyelination with the resulting symptomatic consequences.Tags: