Document Detail


Microglia-derived nerve growth factor causes cell death in the developing retina.
MedLine Citation:
PMID:  9459440     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
While nerve growth factor (NGF) is best known for its trophic functions, recent experiments indicate that it can also cause cell death during development by activating the neurotrophin receptor p75. We now identify microglial cells as the source of NGF as a killing agent in the developing eye. When the retina is separated from the surrounding tissue before colonization by microglial cells, no NGF can be detected, and cell death is dramatically reduced. It is restored by the addition of microglial cells, an effect that is blocked by NGF antibodies. NGF adsorbed at the surface of beads, but not soluble NGF, mimics the killing action of microglial cells. These results indicate an active role for macrophages in neuronal death.
Authors:
J M Frade; Y A Barde
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Neuron     Volume:  20     ISSN:  0896-6273     ISO Abbreviation:  Neuron     Publication Date:  1998 Jan 
Date Detail:
Created Date:  1998-03-09     Completed Date:  1998-03-09     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8809320     Medline TA:  Neuron     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  35-41     Citation Subset:  IM    
Affiliation:
Max-Planck Institute of Neurobiology, Department of Neurobiochemistry, Planegg-Martinsried, Federal Republic of Germany.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Cell Death / physiology
Chick Embryo / cytology,  metabolism,  physiology
Eye / embryology
Immunohistochemistry
Macrophages / physiology
Microglia / metabolism*
Nerve Growth Factors / metabolism,  physiology*
Retina / cytology,  embryology*
Tissue Distribution
Chemical
Reg. No./Substance:
0/Nerve Growth Factors

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Dosage-sensitive and complementary functions of roundabout and commissureless control axon crossing ...
Next Document:  Nonsynaptic glycine receptor activation during early neocortical development.