%0 Journal Article %1 Dommergues2003 %A Dommergues, M-A. %A Plaisant, F. %A Verney, C. %A Gressens, P. %D 2003 %J Neuroscience %K Ani; Animals; Anti-Bacterial Agents; Antigens, CD45; Antirheumatic Brain; Brain Injuries; Cell Count; Death; Cerebral Cortex; Palsy; Chloroquine; Disease Models, Animal; Dose-Response Relationship, Drug; Drug Interacti; Glycoproteins; Ibotenic Acid; Immunohistochemistry; Lectins; Leukemic Infiltration; Macrophage-1 Antigen; Mice; Microglia; Minocycline; Neurons; Neuroprotective Proliferating Nuclear Staining and Labeling; Time Factors; mals, Newborn; ons %N 3 %P 619--628 %T Early microglial activation following neonatal excitotoxic brain damage in mice: a potential target for neuroprotection. %V 121 %X 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).

@article{Dommergues2003, abstract = {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).}, added-at = {2014-07-19T19:22:47.000+0200}, author = {Dommergues, M-A. and Plaisant, F. and Verney, C. and Gressens, P.}, biburl = {https://www.bibsonomy.org/bibtex/21eeac63860a181304be0bae93af245a9/ar0berts}, groups = {public}, interhash = {387e76924f64d338ec6f0b2a98bf7200}, intrahash = {1eeac63860a181304be0bae93af245a9}, journal = {Neuroscience}, keywords = {Ani; Animals; Anti-Bacterial Agents; Antigens, CD45; Antirheumatic Brain; Brain Injuries; Cell Count; Death; Cerebral Cortex; Palsy; Chloroquine; Disease Models, Animal; Dose-Response Relationship, Drug; Drug Interacti; Glycoproteins; Ibotenic Acid; Immunohistochemistry; Lectins; Leukemic Infiltration; Macrophage-1 Antigen; Mice; Microglia; Minocycline; Neurons; Neuroprotective Proliferating Nuclear Staining and Labeling; Time Factors; mals, Newborn; ons}, number = 3, pages = {619--628}, pii = {S030645220300558X}, pmid = {14568022}, timestamp = {2014-07-19T19:22:47.000+0200}, title = {Early microglial activation following neonatal excitotoxic brain damage in mice: a potential target for neuroprotection.}, username = {ar0berts}, volume = 121, year = 2003 }