Oligodendrocytes are cells in the central nervous system (CNS) responsible for the process of myelination.
They myelinate multiple axons, with an average of approximately ten axons per oligodendrocyte.
They have the ability to sense the health and status of the axons they myelinate.
Schwann cells are found in the peripheral nervous system (PNS) and myelinate axons at a 1:1 ratio (one Schwann cell for each axon).
Myelination correlates with axonal diameter; larger axons typically have thicker myelin sheaths.
Schwann cells play a crucial role in supporting and nourishing axons, and they also differentiate into types involved in neuromuscular junctions.
Myelin is a multi-layered insulating sheath that enhances the speed of electrical conduction along axons.
Nodes of Ranvier are gaps in the myelin sheath where action potentials are propagated.
The g-ratio, which describes the number of myelin layers, is consistently about ten layers per axon across both CNS and PNS.
There is interdependence between myelin-producing cells (oligodendrocytes and Schwann cells) and the axons they myelinate.
Loss of axons leads to degeneration of oligodendrocytes; damaged axons cannot be remyelinated.
OBCs exist at the interface between the PNS and CNS, specifically in the olfactory bulb, guiding axons towards the olfactory epithelium.
They exhibit phagocytic abilities and can remove axonal debris, playing a role similar to microglia in the system.
OBCs secrete neurotrophic factors and possess markers indicative of their function and developmental lineage.
Myelination occurs through a developmental process tied to the growth of axons; oligodendrocytes respond to signals from mature axons.
Initial contact between oligodendrocytes and axons leads to oligodendrocyte differentiation and expression of myelination proteins.
The structural organization of myelin includes multiple layers and specific molecular patterns that maintain functional compartments like the nodes of Ranvier.
Myelin consists of approximately 70% lipids (mainly cholesterol, phospholipids, and glycolipids) and 30% proteins.
Key myelin proteins include myelin binding protein, PLP, P0, and MAG, which facilitate the fusing of myelin layers and retention of axons.
Multiple sclerosis (MS) involves autoimmune responses attacking myelin, primarily in white matter areas like the spinal cord and cerebellum.
The disease goes through relapses and remissions characterized by demyelination and attempts at remyelination.
The blood-brain barrier breakdown allows autoreactive T-cells and antibodies to enter the CNS, perpetuating inflammatory cycles.
Chronic phases engage microglia and promote further damage, leading to axonal degeneration, while some neuroprotective activity occurs from oligodendrocyte precursor cells attempting to remyelinate damaged axons.
Initiation involves T-cell driven inflammation causing myelin degradation, leading to axonal vulnerability; this creates a cycle of immune reactivation exacerbated by debris in the CNS.
MRI scans can show active versus chronic lesions in MS patients, reflecting the dynamic nature of myelin integrity during the disease progression.
Key concepts covered include the functions of oligodendrocytes and Schwann cells, the importance of myelin in neuronal signaling, and the impact of demyelinating diseases on these processes.