Under the Ranvier lacing rings the neurologist understands the exposed areas of axons. The lacing rings thus play an important role in the saltatory conduction of excitation and in the generation of action potentials. In demyelinating diseases this saltatory conduction of excitation is disturbed.
The Ranvier lacing rings are part of the nerves. They occur in the central as well as in the peripheral nervous system and are one of the most important components of the saltatory conduction. Without the Ranvier tie-rings, nerve conduction speed of 60 m / s would be inconceivable, as is the case with the A-alpha nerve fibers of the motor nervous system.Several Schwann cells are wrapped around a nerve fiber.
The Ranvier rings are the exposed parts of the axons where two Schwann cells or glial cells meet. The axons of nerves are surrounded by a pithy layer of myelin. This layer electrically isolates the nerves and increases their conductivity. The myelin is interrupted at the location of the Ranvier laced rings. The lacing rings were named after the anatomist Ranvier, who first described the anatomical structures in the 19th century.
The rings are around one μm long and occur every one to two millimeters along the axon. Between them there is a so-called internode. This is the myelated section of the axon, which is isolated in the central nervous system with glial cells and in the peripheral nervous system with Schwann cells.
In the area of the laced rings, the cell membrane has a high density and contains voltage-controlled sodium channels. At these points, however, it is not isolated from the environment with Schwann cells or glial cells. The axon and the glial cells or Schwann cells are connected on the sides of the constriction ring by paranodal septum connections, i.e. by narrow bands of membrane potential. This creates a closed space, the biochemical milieu of which can be regulated independently of the environment.
The Ranvier lacing rings primarily fulfill a task as part of the saltatory excitation conduction. This saltatory excitation conduction enables the rapid excitation of nerve fibers and ensures the prompt transmission of an action potential.
Thick nerve fibers are generally more conductive than thin branches. The principle of saltatory excitation conduction ensures that the conduction speed of thin branches is still sufficient. An action potential therefore does not run continuously along the axons, but jumps from one cord ring to the next. Between the rings lies the isolated internode, which electrotonically transmits the excitation. The myelinated part of the axon is electrically isolated from its surroundings, similar to a plastic cable.
The lacing rings are the interruptions in this insulation, in which the potential for action arises. When such an action potential is present, the axon's sodium channels open. A stream of Na + ions flows into the axon and exits at the next cone. With the help of this ion current, the action potential can depolarize the subsequent axon enough to trigger an action potential there too. The excitation arises accordingly only at the laced rings, whereby the myelinated parts of the axons are skipped, so to speak.
A nerve cell has a certain resting membrane potential in a non-excited state. A potential difference occurs between their extra and intracellular space. But there is no difference along the axon. When excitation occurs on one of the laced rings, the membrane is depolarized beyond the threshold potential. Since the Na + channels are voltage dependent, they open. This means that Na + ions flow from the extracellular space into the intracellular space. The plasma membrane depolarizes around the ring and the capacitor of the membrane is reloaded.
Due to the positive sodium ions, there is an excess of positive charge carriers intracellularly on the ring. An electric field and a potential difference occur along the axon. On the next ring, negative particles are attracted by the positive charge on the first ring and vice versa. Because of these charge shifts, the membrane potential of the second lace ring is also positive.
The Ranvier laces are rarely affected by diseases themselves. Instead, the principle of the saltatory conduction of excitation can be disturbed by so-called demyelinating diseases. Demyelinating diseases break down the insulating myelin around the axons of the nerves. This means that the nerve tracts are no longer electrically isolated and can therefore not fulfill the function of a plastic cable.
As a consequence of this, the transmission of the action potential via the Ranvier tie rings fails. The rings themselves can still fulfill their function, but the potential that is passed on is too weak to trigger any potential for action in the subsequent poker rings. The most well-known disease from the field of demyelinating diseases is the degenerative disease multiple sclerosis. In this autoimmune disease, your own immune system breaks down the myelin of the central nervous system bit by bit. Sensitivity disorders and paralysis can occur as a result of the impaired conduction of excitation.
Polyneuropathies have similar effects on the peripheral nervous system. There are toxic, metabolic, genetic, and infectious polyneuropathies. A tick bite, for example, can precede a polyneuropathy. Diseases such as diabetes or leprosy can also be related to the disease. Alcoholism or malnutrition can also trigger polyneuropathies.
The same applies to disorders of the protein balance and vitamin intake disorders. Apart from that, polyneuropathy also occurs in almost a third of all cases in the context of tumor diseases. Unlike multiple sclerosis, polyneuropathies do not break down the myelin of the central nervous system, but damage the nerve tracts of the peripheral nervous system.