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Related Concept Videos

Nervous Tissue: Myelin01:25

Nervous Tissue: Myelin

The myelin sheath is a multilayered lipid and protein covering that insulates the axon of a neuron, enhancing the speed of nerve impulse conduction. Axons without this sheath are referred to as unmyelinated. Two types of neuroglia, Schwann cells in the peripheral nervous system (PNS) and oligodendrocytes in the central nervous system (CNS) are responsible for producing myelin sheaths.
Schwann cells begin to form myelin sheaths around axons during fetal development. They wrap around a small...
Neurogenesis and Regeneration of Nervous Tissue01:15

Neurogenesis and Regeneration of Nervous Tissue

In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...
Nervous Tissue: Glial Cells01:31

Nervous Tissue: Glial Cells

Glia, or neuroglia, are vital support cells that assist neurons in their functions. The term "glia" originates from the Greek word for "glue," reflecting their role in holding the nervous system together. These cells can be categorized into six types: four in the central nervous system (CNS) and two in the peripheral nervous system (PNS).
The CNS glial cell includes the astrocytes, the oligodendrocytes, the microglia, and the ependymal cells.
Astrocytes are star-shaped glial cells that interact...
Glial Cells01:04

Glial Cells

Overview

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Related Experiment Video

Updated: May 25, 2026

Generation of Oligodendrocytes and Oligodendrocyte-Conditioned Medium for Co-Culture Experiments
09:05

Generation of Oligodendrocytes and Oligodendrocyte-Conditioned Medium for Co-Culture Experiments

Published on: February 9, 2020

[Demyelination and oligodendrocytes].

Takayuki Itoh1, Makoto Horiuchi, Kouji Wakayama

  • 1Department of Neurology/Shriners Hospitals for Children Northern California, University of California Davis, School of Medicine, USA.

Rinsho Shinkeigaku = Clinical Neurology
|January 27, 2012
PubMed
Summary
This summary is machine-generated.

Neuroinflammation can impair oligodendrocyte progenitor cell (OPC) regeneration, leading to remyelination failure. Interferon regulatory factors (IRFs) are implicated in gamma-interferon

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Rapid and Specific Immunomagnetic Isolation of Mouse Primary Oligodendrocytes

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Last Updated: May 25, 2026

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Published on: March 20, 2019

Rapid and Specific Immunomagnetic Isolation of Mouse Primary Oligodendrocytes
09:32

Rapid and Specific Immunomagnetic Isolation of Mouse Primary Oligodendrocytes

Published on: May 21, 2018

Area of Science:

  • Neuroscience
  • Cell Biology
  • Immunology

Context:

  • The central nervous system's limited regeneration contrasts with adult oligodendrocyte progenitor cells' (OPCs) robust regenerative capacity.
  • Remyelination failure, particularly after recurrent neuroinflammation, hinders functional recovery in neurological disorders.
  • Oligodendroglial progenitor cells (OPCs) are crucial for remyelination following demyelination.

Purpose:

  • To investigate the molecular mechanisms underlying gamma-interferon-induced cytotoxicity in OPCs.
  • To identify key transcription factors mediating gamma-interferon's detrimental effects on OPCs.
  • To differentiate the effects of gamma-interferon and beta-interferon on OPCs.

Summary:

  • Gamma-interferon, a proinflammatory cytokine, induces OPC death, inhibiting proliferation and differentiation, contributing to remyelination failure.
  • Beta-interferon, a therapeutic agent for multiple sclerosis, does not induce OPC death.
  • Interferon regulatory factors 1 and 8 (IRF1 and IRF8) are identified as candidate transcription factors responsible for gamma-interferon-mediated OPC cytotoxicity.

Impact:

  • Findings provide insights into the molecular basis of remyelination failure in neuroinflammatory conditions.
  • Identification of IRF1 and IRF8 offers potential therapeutic targets for enhancing remyelination.
  • Further validation in in vivo models is crucial for understanding and treating remyelination failure.