Skip to main content

Main menu

  • HOME
  • CONTENT
    • Early Release
    • Featured
    • Current Issue
    • Issue Archive
    • Collections
    • Podcast
  • ALERTS
  • FOR AUTHORS
    • Information for Authors
    • Fees
    • Journal Clubs
    • eLetters
    • Submit
  • EDITORIAL BOARD
  • ABOUT
    • Overview
    • Advertise
    • For the Media
    • Rights and Permissions
    • Privacy Policy
    • Feedback
  • SUBSCRIBE

User menu

  • Log in
  • My Cart

Search

  • Advanced search
Journal of Neuroscience
  • Log in
  • My Cart
Journal of Neuroscience

Advanced Search

Submit a Manuscript
  • HOME
  • CONTENT
    • Early Release
    • Featured
    • Current Issue
    • Issue Archive
    • Collections
    • Podcast
  • ALERTS
  • FOR AUTHORS
    • Information for Authors
    • Fees
    • Journal Clubs
    • eLetters
    • Submit
  • EDITORIAL BOARD
  • ABOUT
    • Overview
    • Advertise
    • For the Media
    • Rights and Permissions
    • Privacy Policy
    • Feedback
  • SUBSCRIBE
PreviousNext
ARTICLE, Development/Plasticity/Repair

Late Oligodendrocyte Progenitors Coincide with the Developmental Window of Vulnerability for Human Perinatal White Matter Injury

Stephen A. Back, Ning Ling Luo, Natalya S. Borenstein, Joel M. Levine, Joseph J. Volpe and Hannah C. Kinney
Journal of Neuroscience 15 February 2001, 21 (4) 1302-1312; DOI: https://doi.org/10.1523/JNEUROSCI.21-04-01302.2001
Stephen A. Back
1Department of Pediatrics, Oregon Health Sciences University, Portland, Oregon 97201,
3Neurology and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Ning Ling Luo
1Department of Pediatrics, Oregon Health Sciences University, Portland, Oregon 97201,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Natalya S. Borenstein
3Neurology and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Joel M. Levine
2Department of Neurobiology and Behavior, State University of New York, Stony Brook, New York 11794, and the Departments of
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Joseph J. Volpe
3Neurology and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Hannah C. Kinney
3Neurology and
4Pathology, Children's Hospital and Harvard Medical School, Boston, Massachusetts 02115
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF
Loading

Abstract

Hypoxic-ischemic injury to the periventricular cerebral white matter [periventricular leukomalacia (PVL)] results in cerebral palsy and is the leading cause of brain injury in premature infants. The principal feature of PVL is a chronic disturbance of myelination and suggests that oligodendrocyte (OL) lineage progression is disrupted by ischemic injury. We determined the OL lineage stages at risk for injury during the developmental window of vulnerability for PVL (23–32 weeks, postconceptional age). In 26 normal control autopsy human brains, OL lineage progression was defined in parietal white matter, a region of predilection for PVL. Three successive OL stages, the late OL progenitor, the immature OL, and the mature OL, were characterized between 18 and 41 weeks with anti-NG2 proteoglycan, O4, O1, and anti-myelin basic protein (anti-MBP) antibodies. NG2+O4+ late OL progenitors were the predominant stage throughout the latter half of gestation. Between 18 and 27 weeks, O4+O1+ immature OLs were a minor population (9.9 ± 2.1% of total OLs; n = 9). Between 28 and 41 weeks, an increase in immature OLs to 30.9 ± 2.1% of total OLs (n = 9) was accompanied by a progressive increase in MBP+ myelin sheaths that were restricted to the periventricular white matter. The developmental window of high risk for PVL thus precedes the onset of myelination and identifies the late OL progenitor as the major potential target. Moreover, the decline in incidence of PVL at ∼32 weeks coincides with the onset of myelination in the periventricular white matter and suggests that the risk for PVL is related to the presence of late OL progenitors in the periventricular white matter.

  • development
  • cell lineage
  • cerebral white matter
  • cerebral cortex
  • myelination
  • O4 antibody
  • O1 antibody
  • NG2
  • myelin basic protein
  • immunohistochemistry
  • neurofilament protein
  • microglia
  • periventricular leukomalacia
  • prematurity
View Full Text
Back to top

In this issue

The Journal of Neuroscience: 21 (4)
Journal of Neuroscience
Vol. 21, Issue 4
15 Feb 2001
  • Table of Contents
  • Index by author
Email

Thank you for sharing this Journal of Neuroscience article.

NOTE: We request your email address only to inform the recipient that it was you who recommended this article, and that it is not junk mail. We do not retain these email addresses.

Enter multiple addresses on separate lines or separate them with commas.
Late Oligodendrocyte Progenitors Coincide with the Developmental Window of Vulnerability for Human Perinatal White Matter Injury
(Your Name) has forwarded a page to you from Journal of Neuroscience
(Your Name) thought you would be interested in this article in Journal of Neuroscience.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Print
View Full Page PDF
Citation Tools
Late Oligodendrocyte Progenitors Coincide with the Developmental Window of Vulnerability for Human Perinatal White Matter Injury
Stephen A. Back, Ning Ling Luo, Natalya S. Borenstein, Joel M. Levine, Joseph J. Volpe, Hannah C. Kinney
Journal of Neuroscience 15 February 2001, 21 (4) 1302-1312; DOI: 10.1523/JNEUROSCI.21-04-01302.2001

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Respond to this article
Request Permissions
Share
Late Oligodendrocyte Progenitors Coincide with the Developmental Window of Vulnerability for Human Perinatal White Matter Injury
Stephen A. Back, Ning Ling Luo, Natalya S. Borenstein, Joel M. Levine, Joseph J. Volpe, Hannah C. Kinney
Journal of Neuroscience 15 February 2001, 21 (4) 1302-1312; DOI: 10.1523/JNEUROSCI.21-04-01302.2001
del.icio.us logo Digg logo Reddit logo Twitter logo CiteULike logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
    • Abstract
    • MATERIALS AND METHODS
    • RESULTS
    • DISCUSSION
    • Footnotes
    • REFERENCES
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF

Keywords

  • development
  • cell lineage
  • cerebral white matter
  • cerebral cortex
  • myelination
  • O4 antibody
  • O1 antibody
  • NG2
  • myelin basic protein
  • immunohistochemistry
  • neurofilament protein
  • microglia
  • periventricular leukomalacia
  • prematurity

Responses to this article

Respond to this article

Jump to comment:

No eLetters have been published for this article.

Related Articles

Cited By...

More in this TOC Section

ARTICLE

  • Cytoskeletal and Morphological Alterations Underlying Axonal Sprouting after Localized Transection of Cortical Neuron AxonsIn Vitro
  • Developmental Increase in Vesicular Glutamate Content Does Not Cause Saturation of AMPA Receptors at the Calyx of Held Synapse
  • Aberrant Chloride Transport Contributes to Anoxic/Ischemic White Matter Injury
Show more ARTICLE

Development/Plasticity/Repair

  • A Unique “Reversed” Migration of Neurons in the Developing Claustrum
  • Post-synaptic NMDA Receptor Expression Is Required for Visual Corticocollicular Projection Refinement in the Mouse Superior Colliculus
  • Spatiotemporal Developmental Gradient of Thalamic Morphology, Microstructure, and Connectivity fromthe Third Trimester to Early Infancy
Show more Development/Plasticity/Repair
  • Home
  • Alerts
  • Visit Society for Neuroscience on Facebook
  • Follow Society for Neuroscience on Twitter
  • Follow Society for Neuroscience on LinkedIn
  • Visit Society for Neuroscience on Youtube
  • Follow our RSS feeds

Content

  • Early Release
  • Current Issue
  • Issue Archive
  • Collections

Information

  • For Authors
  • For Advertisers
  • For the Media
  • For Subscribers

About

  • About the Journal
  • Editorial Board
  • Privacy Policy
  • Contact
(JNeurosci logo)
(SfN logo)

Copyright © 2023 by the Society for Neuroscience.
JNeurosci Online ISSN: 1529-2401

The ideas and opinions expressed in JNeurosci do not necessarily reflect those of SfN or the JNeurosci Editorial Board. Publication of an advertisement or other product mention in JNeurosci should not be construed as an endorsement of the manufacturer’s claims. SfN does not assume any responsibility for any injury and/or damage to persons or property arising from or related to any use of any material contained in JNeurosci.