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Myelination
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Myelination
Myelination, or myelinogenesis, is the formation and development of myelin sheaths in the nervous system, typically initiated in late prenatal neurodevelopment and continuing throughout postnatal development. The term myelinogenesis is also sometimes used to differentiate the very early stages of embryonic myelination.
Myelin is formed by oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system. Myelination continues throughout the lifespan to support learning and memory via neural circuit plasticity as well as remyelination following injury. Successful myelination of axons increases action potential speed by enabling saltatory conduction, which is essential for timely signal conduction between spatially separate brain regions, as well as provides metabolic support to neurons.
Myelin is formed by oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system. Therefore, the first stage of myelinogenesis is often defined as the differentiation of oligodendrocyte progenitor cells (OPCs) or Schwann cell progenitors into their mature counterparts, followed by myelin formation around axons.
The oligodendrocyte lineage can be further classified into four stages based on their relation to the onset of myelination:
Myelinogenesis thus encompasses the process of transition between phases 3 and 4. Upon initiation of myelinogenesis, each pioneer process forms lamellar extensions which extend and elaborate circumferentially around the target axon. This forms the first turn of the myelin sheath. The sheath continues to expand along the length of the target axon while new membrane is synthesized at the leading edge of the inner tongue of the developing myelin sheath, which begins to take on a spiral cross-sectional structure.
To drive proper assembly of membrane layers, PLP is inserted into the membrane to stabilize interactions between external leaflets of the myelin membranes; MBP is locally translated and inserted into the cytoplasmic membrane leaflets to strengthen myelin membranes internally. In concert with the formation of axonal nodes of Ranvier, the myelin sheath's edges form paranodal loops.
The basic helix–loop–helix transcription factor OLIG1 plays an integral role in the process of oligodendrocyte myelinogenesis by regulating expression of myelin-related genes. OLIG1 is necessary in order to initiate myelination by oligodendrocytes in the brain, but is somewhat dispensable in the spinal cord.
Axon-derived signals regulate the onset of myelinogenesis. Researchers studied regenerating PNS axons for 28 weeks in order to investigate whether or not peripheral axons stimulate oligodendrocytes to begin myelination. Experimental induction of myelination by regenerating peripheral axons demonstrated that Schwann cells and oligodendrocytes have a shared mechanism to stimulate myelination. A similar study working to provide evidence for neuronal regulation of myelinogenesis suggested that myelin formation was due to Schwann cells that were controlled by an undefined property of an associated axon.
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Myelination
Myelination, or myelinogenesis, is the formation and development of myelin sheaths in the nervous system, typically initiated in late prenatal neurodevelopment and continuing throughout postnatal development. The term myelinogenesis is also sometimes used to differentiate the very early stages of embryonic myelination.
Myelin is formed by oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system. Myelination continues throughout the lifespan to support learning and memory via neural circuit plasticity as well as remyelination following injury. Successful myelination of axons increases action potential speed by enabling saltatory conduction, which is essential for timely signal conduction between spatially separate brain regions, as well as provides metabolic support to neurons.
Myelin is formed by oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system. Therefore, the first stage of myelinogenesis is often defined as the differentiation of oligodendrocyte progenitor cells (OPCs) or Schwann cell progenitors into their mature counterparts, followed by myelin formation around axons.
The oligodendrocyte lineage can be further classified into four stages based on their relation to the onset of myelination:
Myelinogenesis thus encompasses the process of transition between phases 3 and 4. Upon initiation of myelinogenesis, each pioneer process forms lamellar extensions which extend and elaborate circumferentially around the target axon. This forms the first turn of the myelin sheath. The sheath continues to expand along the length of the target axon while new membrane is synthesized at the leading edge of the inner tongue of the developing myelin sheath, which begins to take on a spiral cross-sectional structure.
To drive proper assembly of membrane layers, PLP is inserted into the membrane to stabilize interactions between external leaflets of the myelin membranes; MBP is locally translated and inserted into the cytoplasmic membrane leaflets to strengthen myelin membranes internally. In concert with the formation of axonal nodes of Ranvier, the myelin sheath's edges form paranodal loops.
The basic helix–loop–helix transcription factor OLIG1 plays an integral role in the process of oligodendrocyte myelinogenesis by regulating expression of myelin-related genes. OLIG1 is necessary in order to initiate myelination by oligodendrocytes in the brain, but is somewhat dispensable in the spinal cord.
Axon-derived signals regulate the onset of myelinogenesis. Researchers studied regenerating PNS axons for 28 weeks in order to investigate whether or not peripheral axons stimulate oligodendrocytes to begin myelination. Experimental induction of myelination by regenerating peripheral axons demonstrated that Schwann cells and oligodendrocytes have a shared mechanism to stimulate myelination. A similar study working to provide evidence for neuronal regulation of myelinogenesis suggested that myelin formation was due to Schwann cells that were controlled by an undefined property of an associated axon.