Neurologists refer to Ranvier’s laced rings as the exposed sites of axons. Thus, the lacing rings play an important role in saltatory excitation conduction and in the generation of action potentials. In demyelinating diseases, this saltatory excitation conduction is impaired.
What are Ranvier’s cord rings?
Ranvier’s cord rings are a component of nerves. They are found in the central nervous system as well as in the peripheral nervous system and are one of the most important components of saltatory excitation conduction. Without the Ranvier rings, nerve conduction velocities of 60 m/s would be unthinkable, as they are maintained by the A-alpha nerve fibers of the motor nervous system. Several Schwann cells are wrapped around each nerve fiber. The Ranvier lacing rings are the exposed portions of axons where two Schwann cells or glial cells meet. The axons of nerves are surrounded by a pithy layer of myelin. This layer electrically insulates the nerves and increases their conductivity. The myelin is interrupted at the site of Ranvier’s lacing rings. The lacing rings were named after the anatomist Ranvier, who first described the anatomical structures in the 19th century.
Anatomy and structure
The lacing rings are about one μm long and occur along the axon about every one to two millimeters. Between each of them is a so-called internode. This is the myelinated section of the axon that is insulated with glial cells in the central nervous system and Schwann cells in the peripheral nervous system. In the region of the cord rings, the cell membrane has a high density and contains voltage-gated sodium channels. However, it is not insulated from the environment with Schwann cells or glial cells at these sites. The axon and glial cells or Schwann cells are joined at the sides of the cord ring by paranodal septal connections, narrow bands of membrane potential. This creates a closed space whose biochemical milieu can be regulated independently of the environment.
Function and tasks
The Ranvier cord rings primarily serve a role as part of 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 generally have better conductivity than thin branches. The principle of saltatory excitation conduction ensures that the conduction velocity of thin branches is nevertheless sufficient. An action potential therefore does not run continuously along the axons, but jumps from one lacing ring to the next. Between the rings lies the insulated internode, which conducts the excitation electrotonically. The myelinated part of the axon is electrically insulated from its surroundings similar to a plastic cable. The lacing rings are the interruptions of this insulation, in which only the action potential arises. When such an action potential is present, the sodium channels of the axon open. A Na+ ion current flows into the axon and exits at the next lacing ring. With the help of this ion current, the action potential can depolarize the subsequent axon sufficiently to trigger an action potential there as well. Thus, excitation occurs only at the lacing rings, skipping the myelinated parts of the axons, so to speak. A nerve cell exhibits a certain resting membrane potential in an unexcited state. A potential difference occurs between its extracellular and intracellular space. However, there is no difference along the axon. When excitation occurs at one of the lacing rings, the membrane is depolarized beyond the threshold potential. Since the Na+ channels are voltage dependent, they open. Thus, Na+ ions flow from the extracellular space into the intracellular space. The plasma membrane depolarizes around the lacing ring and the capacitor of the membrane is recharged. Due to the positive sodium ions, an excess of positive charge carriers is present intracellularly at the lacing ring. An electric field and a potential difference along the axon occur. At the next lacing ring, negative particles are now attracted by the positive charge at the first lacing ring and vice versa. Because of these charge shifts, the membrane potential of the second lacing ring also becomes positive.
Diseases
Ranvier lacing rings are themselves rarely affected by disease.For this, the principle of saltatory conduction of excitation may be disturbed by the so-called demyelinating diseases. Demyelinating diseases break down the insulating myelin around the axons of the nerves. As a result, the nerve tracts are no longer electrically insulated and thus cannot perform the function of a plastic cable. As a consequence, the transmission of the action potential via the Ranvier lacing rings also fails. The rings themselves can still fulfill their function, but the forwarded potential is too weak to trigger any action potential at all at the subsequent poker rings. The best-known disease in the field of demyelinating diseases is the degenerative disease multiple sclerosis. In this autoimmune disease, the patient’s own immune system breaks down the myelin of the central nervous system piece by piece. Sensory disturbances and paralysis can develop 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. For example, a polyneuropathy may be preceded by a tick bite. Diseases such as diabetes or leprosy may also be associated with the condition. Likewise, alcoholism or malnutrition can trigger polyneuropathies. The same applies to disorders of the protein balance and vitamin absorption disorders. Apart from this, polyneuropathy also occurs in almost one third of all cases 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.
