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@@ -74,8 +74,8 @@ description: |
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protects against cognitive impairment induced by experimental perinatal asphyxia. To investigate the
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long-term neuropathological effects of hypoxic-ischemic injury to the developing brain and the role
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of C3aR signaling therein, we subjected wildtype mice, C3aR deficient mice, and mice expressing
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- biologically active C3a in the CNS to mild hypoxic-ischemic brain injury on postnatal day 9.
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- We found that such injury triggers neurodegeneration and pronounced reactive gliosis in the ipsilesional
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+ biologically active C3a in the CNS to mild hypoxic-ischemic brain injury on postnatal day 9. We found
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+ that such injury triggers neurodegeneration and pronounced reactive gliosis in the ipsilesional
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hippocampus both of which persist long into adulthood. Transgenic expression of C3a in reactive astrocytes
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reduced hippocampal neurodegeneration and reactive gliosis. In contrast, neurodegeneration and microglial
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cell density increased in mice lacking C3aR. Intranasal administration of C3a for 3 days starting
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