Through the Saltatory conduction of excitation the sufficiently fast conduction speed of nerve tracts is ensured for vertebrates. Action potentials jump from one unisolated ring to the next on the isolated axons. In demyelinating diseases, the isolating myelin is broken down, which disrupts the conduction of excitation.
The saltatory conduction of excitation ensures that the conduction speed of nerve tracts is sufficiently fast for vertebrates.
The saltatory conduction of excitation is a form of nerve conductivity. In the organism of vertebrates, nerve fibers are electrically isolated from their environment by myelin sheath and thus take on the function of a sheathed cable. The excitation of a nerve fiber occurs at the interruptions in this insulating layer, which are also known as tying rings or knots.
Many vertebrate nerve fibers are thin in shape. Thin axons have a lower conduction velocity than strong nerve tracts. So that the conduction speed of the nerves is sufficient despite the low strength, the excitation conduction of the vertebrates is built up saltatory and uses both biochemical and bioelectrical processes to transmit action potentials.
The action potential jumps from one ring to the other in this type of conduction and leaves out the sheathed parts of the axons. With this principle, a higher conduction speed is achieved through voltage-dependent sodium pumps and bioelectrical biochemical processes.
In the peripheral nervous system, Schwann's cells form the myelin that surrounds the nerves. Oligodendrocytes take on this task in the central nervous system. Axons in both systems are coated with myelin, which has an electrically insulating effect. The isolation of the axons is interrupted at a distance of between 0.2 and 1.5 millimeters. These breaks are also known as knots or Ranvier ties. The myelin-sheathed sections, on the other hand, are called internodes and ensure a reduced membrane time constant, which ensures a conduction speed of 100 meters per second. There are also voltage-dependent sodium + channels in the sheathless lacing rings.
As long as an axon is not excited, the so-called resting potential prevails in its node and along its internode. Between the intracellular space and the extracellular space of the axon there is a potential difference with the resting potential. When an action potential is generated on the first cone of the excitation line, which depolarizes its membrane beyond its threshold potential, the voltage-dependent Na + channels open. Due to electrochemical properties, Na + ions then flow from the extracellular space into the intracellular space.
The plasma membrane is depolarized at the level of the cone ring and the membrane capacitor is recharged within 0.1 ms. In the area of the lace ring, there is an intracellular excess of positive charge carriers compared to the surroundings because of the sodium ions flowing in. An electric field is created. This field generates a potential difference along the axon and has an influence on charged parts in the closest distance.
The negatively charged particles on the next ring are attracted to the excess positive charge in the first ring. Positively charged particles between the first and second constriction rings move towards the second node. These charge shifts positively affect the membrane potential of the second cone ring, although the ions have not reached it. In this way, the excitation jumps from ring to ring and retains the property of sufficiently depolarizing the membrane of the subsequent rings.
Demyelinating diseases break down the myelin sheaths around nerve fibers. These myelin sheaths are a prerequisite for the saltatory conduction of excitation. Without the myelin sheath, high current losses occur in the internode. Therefore, greater excitations are required so that the axons can depolarize the next cording rings via an action potential.
As a rule, the action potential transmitted after the losses is too low to be recognized as such by the next node. As a result, the lace ring does not pass the excitement on.
The phenomenon of demyelination is also known as demyelination and belongs to the degenerative diseases. Age-related processes as well as toxic and inflammatory processes can demark the axons and thus endanger the saltatory transmission of action potentials.
Vitamin deficiencies can also be related to this phenomenon. Too little vitamin B6 and vitamin B12 in particular is associated with discoloration. Such a vitamin deficiency is often found in alcoholism, for example. A demyelination of the nervous system can also occur in the context of drug abuse.
The most well-known inflammatory cause of demixing of the nerves is the autoimmune disease multiple sclerosis. The own immune system destroys nerve tissue in the central nervous system as part of the disease. Other causes of demarking can be diabetes, Lyme disease or genetic diseases. The genetic diseases with demyelinating properties include, for example, Krabbe's disease, Pelizaeus-Merzbacher's disease and Déjérine-Sottas syndrome.
The symptoms that arise with demyelinating of the nerve tissue depend on the location of the demyelinating foci. In the central nervous system, for example, demyelinating can lead to an impairment of the sensory organs, above all to an impairment of the eyes. Paralysis is also conceivable with demyelinating in the central nervous system, since the motor nerve tracts and their control centers are located there. In the peripheral nervous system, demyelinating of the nerves is less often associated with paralysis. Instead, the demyelination of peripheral axons can lead to numbness or other sensory disorders.
The diagnosis of demyelinating disease is made using imaging techniques such as magnetic resonance imaging. The MRI images typically show white foci of demyelinating when contrast agent is administered.