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Remyelination is the process of propagating oligodendrocyte precursor cells to form oligodendrocytes to create new myelin sheaths on demyelinated axons in the Central nervous system (CNS). This is a process naturally regulated in the body and tends to be very efficient in a healthy CNS. [ 1 ]
When a nerve axon is severed, the end still attached to the cell body is labeled the proximal segment, while the other end is called the distal segment. After injury, the proximal end swells and experiences some retrograde degeneration, but once the debris is cleared, it begins to sprout axons and the presence of growth cones can be detected.
The implementation of this method of study has long allowed for experimental observation of myelinogenesis in a model organism nerve that consists entirely of unmyelinated axons. Furthermore, the use of the rat optic nerve helped provide insight for early myelinogenesis researchers into improper and atypical courses of myelinogenesis.
The loss or lack of OPCs, and consequent lack of differentiated oligodendrocytes, is associated with a loss of myelination and subsequent impairment of neurological functions. [3] In addition, OPCs express receptors for various neurotransmitters and undergo membrane depolarization when they receive synaptic inputs from neurons.
Myelin (/ ˈ m aɪ. ə l ɪ n / MY-ə-lin) is a lipid-rich material that surrounds nerve cell axons to insulate them and increase the rate at which electrical impulses (called action potentials) pass along the axon. [1] [2] The myelinated axon can be likened to an electrical wire (the axon) with insulating material (myelin) around it. However ...
A single oligodendrocyte can extend its processes to cover up to 40 axons, that can include multiple adjacent axons. [2] The myelin sheath is not continuous but is segmented along the axon's length at gaps known as the nodes of Ranvier. In the peripheral nervous system the myelination of axons is carried out by Schwann cells. [1]
Since an axon can be unmyelinated or myelinated, the action potential has two methods to travel down the axon. These methods are referred to as continuous conduction for unmyelinated axons, and saltatory conduction for myelinated axons. Saltatory conduction is defined as an action potential moving in discrete jumps down a myelinated axon.
To be specific, MS involves the loss of oligodendrocytes, the cells responsible for creating and maintaining a fatty layer—known as the myelin sheath—which helps the neurons carry electrical signals (action potentials). [1] This results in a thinning or complete loss of myelin, and as the disease advances, the breakdown of the axons of