Saltatory excitation conduction ensures sufficiently fast conduction velocity of neural pathways for vertebrates. Action potentials jump from one unisolated cord ring to the next on isolated axons. In demyelinating diseases, the insulating myelin is degraded, disrupting excitation conduction.
What is saltatory excitation conduction?
Saltatory excitation conduction ensures sufficiently fast conduction velocity of neural pathways for vertebrates. Saltatory excitation conduction is a form of nerve conduction. In the vertebrate organism, nerve fibers are electrically insulated from their surroundings by myelin sheaths, thus performing the function of a sheathed cable. The excitation of a nerve fiber occurs at the interruptions of this insulating layer, which are also called lacing rings or knots. Many vertebrate nerve fibers are thin in shape. Thin axons have a slower conduction velocity than stout nerve fibers. To ensure that the conduction velocity of nerves is sufficient despite their thinness, vertebrate excitation conduction is saltatory in nature and makes use of both biochemical and bioelectrical processes to transmit action potentials. In this type of excitation conduction, the action potential jumps from one cord ring to another, leaving out the sheathed portions of the axons. Voltage-dependent sodium pumping and bioelectrical biochemical processes are used to achieve higher conduction velocity with this principle.
Function and task
In the peripheral nervous system, Schwann cells form the myelin that coats nerves. Oligodendrocytes perform this task in the central nervous system. Axons in both systems are sheathed with myelin, which has an electrically insulating effect. The insulation of the axons is interrupted at a distance of between 0.2 and 1.5 millimeters. These interruptions are also called nodes or Ranvier’s lacing rings. In contrast, the myelin sheathed sections are called internodes and provide a reduced membrane time constant that ensures a conduction velocity of 100 meters per second. The sheathless lacing rings also contain voltage-gated sodium+ channels. As long as an axon is not excited, the so-called resting potential prevails in its node and along its internode. A potential difference exists between the intracellular space and the extracellular space of the axon with the resting potential. When an action potential is generated at the first lacing ring of the excitation lead, depolarizing its membrane beyond its threshold potential, the voltage-gated Na+ channels open. Through electrochemical properties, Na+ ions then flow from the extracellular space into the intracellular space. The plasma membrane at the level of the lacing ring depolarizes and the capacitor of the membrane is recharged within 0.1 ms. There is an intracellular excess of positive charge carriers in the area of the lacing ring compared to the surrounding area because of the influx of sodium ions. An electric field is generated. This field generates a potential difference along the axon and has an influence on charged particles at the next distance. The negatively charged particles at the next lacing ring are attracted to the positive charge excess in the first lacing ring. Positively charged particles between the first and second string rings move toward the second node. These charge shifts positively bias the membrane potential of the second lacing ring, even though the ions have not reached it. In this way, the excitation jumps from lacing ring to lacing ring and retains the property of sufficiently depolarizing the membrane of subsequent lacing rings.
Diseases and disorders
Demyelinating diseases degrade the myelin sheaths around nerve fibers. However, these myelin sheaths are a prerequisite for saltatory conduction of excitation. Without the myelin sheath, high current losses occur in the internode. Therefore, it takes larger excitations for the axons to depolarize the next cord rings via an action potential. Usually, after the losses, the transmitted action potential is too small to be recognized as such by the next node. In a consequence, the lacing ring does not transmit the excitation. 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 unmark axons, putting the saltatory transmission of action potentials at risk. Vitamin deficiencies may also be associated with this phenomenon. Specifically, too little vitamin B6 and vitamin B12 is associated with demyelination. Such vitamin deficiency is often present in alcoholism, for example. Demyelination of the nervous system can also occur in the context of drug abuse. The best-known inflammatory cause of demyelination of the nerves is the autoimmune disease multiple sclerosis. The patient’s own immune system destroys nerve tissue in the central nervous system as part of the disease. Other causes of demyelination can be diabetes, Lyme disease or genetic diseases. Genetic diseases with demyelinating properties include, for example, Krabbe disease, Pelizaeus-Merzbacher disease and Déjérine-Sottas syndrome. The symptoms associated with demyelination of nervous tissue depend on the location of the demyelination lesions. In the central nervous system, for example, demyelination can lead to impairment of the sensory organs, especially the eyes. Paralysis is also conceivable in the case of demyelination in the central nervous system, since the motor nerve pathways and their control centers are located there. In the peripheral nervous system, demyelination of the nerves is less frequently associated with paralysis. On the other hand, demyelination of peripheral axons may result in numbness or other sensory disturbances. Diagnosis for demyelinating disease is made using imaging such as magnetic resonance imaging. MRI images typically show white demyelinating foci when contrast is applied.
