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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2003-10-21
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pubmed:abstractText |
Previous studies in a mouse model of neonatal excitotoxic brain damage mimicking the brain lesions in human cerebral palsy showed microglial activation within 24 h after intracerebral injection of the glutamatergic analog ibotenate. Using this model, we studied the expression of CD-45 antigen, a marker of blood-derived cells, by these activated microglial cells labeled by Griffonia simplicifolia I isolectin B4. Immunohistochemistry performed during early development of excitotoxic lesions showed that most cells labeled with the isolectin B4 were CD-45-negative, suggesting that these early activated microglial cells were deriving chiefly from resident microglia and not from circulating monocytes. We also directly tested the hypothesis that activated resident microglia and/or blood-derived monocytes play a role in the pathophysiology of excitotoxic brain damage. Repeated i.p. administrations of chloroquine, chloroquine+colchicine, minocycline, or an anti-MAC1 antibody coupled to the toxin saporin before and/or after ibotenate injection induced a significant reduction in the density of isolectin B4-positive cells. This inhibition of resident microglial and/or blood-derived monocytes activation was accompanied by a significant reduction in the severity of ibotenate-induced brain lesions (up to 79% lesion size reduction with the highest minocycline dose) as well as of ibotenate-induced cortical caspase-3 activation (49% reduction).
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Bacterial Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD45,
http://linkedlifedata.com/resource/pubmed/chemical/Antirheumatic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Chloroquine,
http://linkedlifedata.com/resource/pubmed/chemical/Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Ibotenic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Lectins,
http://linkedlifedata.com/resource/pubmed/chemical/Macrophage-1 Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Minocycline,
http://linkedlifedata.com/resource/pubmed/chemical/Neuroprotective Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Proliferating Cell Nuclear Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/isolectin B4-binding glycoprotein...
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pubmed:status |
MEDLINE
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pubmed:issn |
0306-4522
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
121
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
619-28
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:14568022-Animals,
pubmed-meshheading:14568022-Animals, Newborn,
pubmed-meshheading:14568022-Anti-Bacterial Agents,
pubmed-meshheading:14568022-Antigens, CD45,
pubmed-meshheading:14568022-Antirheumatic Agents,
pubmed-meshheading:14568022-Brain,
pubmed-meshheading:14568022-Brain Injuries,
pubmed-meshheading:14568022-Cell Count,
pubmed-meshheading:14568022-Cell Death,
pubmed-meshheading:14568022-Cerebral Cortex,
pubmed-meshheading:14568022-Cerebral Palsy,
pubmed-meshheading:14568022-Chloroquine,
pubmed-meshheading:14568022-Disease Models, Animal,
pubmed-meshheading:14568022-Dose-Response Relationship, Drug,
pubmed-meshheading:14568022-Drug Interactions,
pubmed-meshheading:14568022-Glycoproteins,
pubmed-meshheading:14568022-Ibotenic Acid,
pubmed-meshheading:14568022-Immunohistochemistry,
pubmed-meshheading:14568022-Lectins,
pubmed-meshheading:14568022-Leukemic Infiltration,
pubmed-meshheading:14568022-Macrophage-1 Antigen,
pubmed-meshheading:14568022-Mice,
pubmed-meshheading:14568022-Microglia,
pubmed-meshheading:14568022-Minocycline,
pubmed-meshheading:14568022-Neurons,
pubmed-meshheading:14568022-Neuroprotective Agents,
pubmed-meshheading:14568022-Proliferating Cell Nuclear Antigen,
pubmed-meshheading:14568022-Staining and Labeling,
pubmed-meshheading:14568022-Time Factors
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pubmed:year |
2003
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pubmed:articleTitle |
Early microglial activation following neonatal excitotoxic brain damage in mice: a potential target for neuroprotection.
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pubmed:affiliation |
INSERM E 9935, Service de Neurologie Pédiatrique, Hôpital Robert-Debré, 48 BD Sérurier, 75019 Paris, France.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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