Special Feature

User Panel

My Panel

My Panel

Bookmark Science Articles

Recent News
Bookmark / Share This Science Site

Immunohistochemical localization of CNTFRalpha in adult mouse retina and optic nerve following intraorbital nerve crush: evidence for the axonal loss of a trophic factor receptor after injury.

Immunohistochemical localization of CNTFRalpha in adult mouse retina and optic nerve following intraorbital nerve crush: evidence for the axonal loss of a trophic factor receptor after injury. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

  • Abstract Text of This Paper
  • Journal Published
  • MeSH Keywords of This Abstract
  • Chemicals and Substances Used in this Paper
  • Grants and Granting Agency of this Research
  • Database Accession Numbers Used in this Paper
  • Related Papers
  • Related Research Tags
  • Rate this Research Paper
  • Immunohistochemical localization of CNTFRalpha in adult mouse retina and optic nerve following intraorbital nerve crush: evidence for the axonal loss of a trophic factor receptor after injury. Abstract Text:

    jill a miotkeJill A Miotke,a john maclennanA John MacLennan,ronald l meyerRonald L Meyer,

    Ciliary neurotrophic factor (CNTF) is important for the survival and outgrowth of retinal ganglion cells (RGCs) in vitro. However, in vivo adult RGCs fail to regenerate and subsequently die following axotomy, even though there are high levels of CNTF in the optic nerve. To address this discrepancy, we used immunohistochemistry to analyze the expression of CNTF receptor alpha (CNTFRalpha) in mouse retina and optic nerve following intraorbital nerve crush. In normal mice, RGC perikarya and axons were intensely labeled for CNTFRalpha. At 24 hours after crush, the immunoreactivity normally seen on axons in the nerve was lost near the lesion. This loss radiated from the crush site with time. At 2 days postlesion, labeled axons were not detected in the proximal nerve, and at 2 weeks were barely detectable in the retina. In the distal nerve, loss of axonal staining progressed to the optic chiasm by 7 days and remained undetectable at 2 weeks. Interfascicular glia in the normal optic nerve were faintly labeled, but by 24 hours after crush they became intensely labeled near the lesion. Double labeling showed these to be both astrocytes and oligodendrocytes. At 7 days postlesion, darkly labeled glia were seen throughout the optic nerve, but at 14 days labeling returned to normal. It is suggested that the loss of CNTFRalpha from axons renders RGCs unresponsive to CNTF, thereby contributing to regenerative failure and death, while its appearance on glia may promote glial scarring.

    Immunohistochemical localization of CNTFRalpha in adult mouse retina and optic nerve following intraorbital nerve crush: evidence for the axonal loss of a trophic factor receptor after injury. Publishing Authors By Initials

    ja miotkeJA Miotke,aj maclennanAJ MacLennan,rl meyerRL Meyer,

    For similar natural sciences: time: time factors research abstracts see: natural sciences: time: time factors research

    PUBMED ID PMID:

    MEDLINE DATE:

    Immunohistochemical localization of CNTFRalpha in adult mouse retina and optic nerve following intraorbital nerve crush: evidence for the axonal loss of a trophic factor receptor after injury. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: The Journal of comparative neurology

    VOLUME: 500

    Page Numbers: 384-400

    Journal Abbreviation: J. Comp. Neurol.

    ISSN: 0021-9967

    DAY: 10

    MONTH: Jan

    YEAR: 2007

    Immunohistochemical localization of CNTFRalpha in adult mouse retina and optic nerve following intraorbital nerve crush: evidence for the axonal loss of a trophic factor receptor after injury. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 406041

    Immunohistochemical localization of CNTFRalpha in adult mouse retina and optic nerve following intraorbital nerve crush: evidence for the axonal loss of a trophic factor receptor after injury. Keywords Mesh Terms:

    KEYWORDS: Time Factors

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Immunohistochemical localization of CNTFRalpha in adult mouse retina and optic nerve following intraorbital nerve crush: evidence for the axonal loss of a trophic factor receptor after injury. Information

    Substance Name: Ciliary Neurotrophic Factor Receptor alp

    Registry Number: 0

    Grant and Affiliation Information for Immunohistochemical localization of CNTFRalpha in adult mouse retina and optic nerve following intraorbital nerve crush: evidence for the axonal loss of a trophic factor receptor after injury.

    AFFILIATION: Department of Developmental and Cell Biology, University of California at Irvine, Irvine, California 92697-2305, USA. jamiotke@uci.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NINDS

    GRANT: NS35224

    ACRONYM: NS

    MEDLINETA: J Comp Neurol

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

    Immunohistochemical localization of CNTFRalpha in adult mouse retina and optic nerve following intraorbital nerve crush: evidence for the axonal loss of a trophic factor receptor after injury Related Publications

     

    Molecular Station USER Menu

    Welcome to Molecular Station!

    You have to register before you can post on our forums or use our advanced features. Register Now! Its Free and Fast!

    Already registered? Login now below.

    User Name:

    Password:

    Already registered and Forgot your password? Click below to recover it.

    Recover Lost Password

    Join now - it's fast and free!

    Molecular Station is THE largest network of researchers, scientists and science lovers anywhere!

    Research Terms of Usage and Disclaimer
    Home
    Features

    Protocols

    DNA Forum

    Science Forum

    DNA Forum
    Biology Forum

    Science News


    [CaRP] XML error: Invalid document end at line 2

    For more click here:Science News