Suppression of microglia activation after hypoxia–ischemia results in age-dependent improvements in neurologic injury

Abstract We previously found increased microglial proliferation and pro-inflammatory cytokine release in infant mice compared to juvenile mice after hypoxia–ischemia (HI). The aim of the current study was to assess for differences in the effect of microglial suppression on HI-induced brain injury in...

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Bibliographic Details
Published in:Journal of neuroimmunology 2016-02, Vol.291, p.18-27
Main Authors: Cikla, Ulas, Chanana, Vishal, Kintner, Douglas B, Covert, Lucia, Dewall, Taylor, Waldman, Alex, Rowley, Paul, Cengiz, Pelin, Ferrazzano, Peter
Format: Article
Language:English
Subjects:
Aging
Allergy and Immunology
Animals
Animals, Newborn
Brain - pathology
Brain Injuries - drug therapy
Brain Injuries - etiology
Brain Injuries - pathology
CD11b Antigen - metabolism
Cerebral atrophy
Disease Models, Animal
Flow Cytometry
Functional Laterality
Hypoxia-Ischemia, Brain - complications
Hypoxia-Ischemia, Brain - pathology
Learning Disabilities - drug therapy
Learning Disabilities - etiology
Leukocyte Common Antigens - metabolism
Magnetic Resonance Imaging
Maze Learning
Mice
Microglia
Microglia - drug effects
Microglia - metabolism
Microglia - pathology
Minocycline - therapeutic use
Neonatal hypoxia–ischemia
Neuroinflammation
Neurologic Examination
Neurology
Statistics, Nonparametric
Time Factors
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Summary:Abstract We previously found increased microglial proliferation and pro-inflammatory cytokine release in infant mice compared to juvenile mice after hypoxia–ischemia (HI). The aim of the current study was to assess for differences in the effect of microglial suppression on HI-induced brain injury in infant and juvenile mice. HI was induced in neonatal (P9) and juvenile (P30) mice and minocycline or vehicle was administered at 2 h and 24 h post-HI. P9 minocycline-treated mice demonstrated early but transient improvements in neurologic injury, while P30 minocycline-treated mice demonstrated sustained improvements in cerebral atrophy and Morris Water Maze performance at 60 days post-HI.
ISSN:0165-5728
1872-8421
DOI:10.1016/j.jneuroim.2015.12.004