scholarly journals Severe Perinatal Hypoxic-Ischemic Brain Injury Induces Long-Term Sensorimotor Deficits, Anxiety-Like Behaviors and Cognitive Impairment in a Sex-, Age- and Task-Selective Manner in C57BL/6 Mice but Can Be Modulated by Neonatal Handling

2019 ◽  
Vol 13 ◽  
Author(s):  
Aida Muntsant ◽  
Kalpana Shrivastava ◽  
Mireia Recasens ◽  
Lydia Giménez-Llort
Keyword(s):  
Cognitive Impairment ◽  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Neonatal Handling ◽  
Sensorimotor Deficits ◽  
Hypoxic Ischemic Brain Injury ◽  
And Task

scholarly journals C3a Receptor Signaling Inhibits Neurodegeneration Induced by Neonatal Hypoxic-Ischemic Brain Injury

2021 ◽  
Vol 12 ◽  
Author(s):  
Andrea Pozo-Rodrigálvarez ◽  
YiXian Li ◽  
Anna Stokowska ◽  
Jingyun Wu ◽  
Verena Dehm ◽  
...  
Keyword(s):  
Brain Injury ◽  
Perinatal Asphyxia ◽  
Brain Inflammation ◽  
Biologically Active ◽  
Reactive Gliosis ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Transgenic Expression ◽  
Hypoxic Ischemic Brain Injury

Hypoxic-ischemic neonatal encephalopathy due to perinatal asphyxia is the leading cause of brain injury in newborns. Clinical data suggest that brain inflammation induced by perinatal insults can persist for years. We previously showed that signaling through the receptor for complement peptide C3a (C3aR) protects against cognitive impairment induced by experimental perinatal asphyxia. To investigate the long-term neuropathological effects of hypoxic-ischemic injury to the developing brain and the role of C3aR signaling therein, we subjected wildtype mice, C3aR deficient mice, and mice expressing biologically active C3a in the CNS to mild hypoxic-ischemic brain injury on postnatal day 9. We found that such injury triggers neurodegeneration and pronounced reactive gliosis in the ipsilesional hippocampus both of which persist long into adulthood. Transgenic expression of C3a in reactive astrocytes reduced hippocampal neurodegeneration and reactive gliosis. In contrast, neurodegeneration and microglial cell density increased in mice lacking C3aR. Intranasal administration of C3a for 3 days starting 1 h after induction of hypoxia-ischemia reduced neurodegeneration and reactive gliosis in the hippocampus of wildtype mice. We conclude that neonatal hypoxic-ischemic brain injury leads to long-lasting neurodegeneration. This neurodegeneration is substantially reduced by treatment with C3aR agonists, conceivably through modulation of reactive gliosis.

Optimization of behavioral testing in a long-term rat model of hypoxic ischemic brain injury

2021 ◽  
Vol 409 ◽  
pp. 113322
Author(s):  
Tayla R. Penny ◽  
Yen Pham ◽  
Amy E. Sutherland ◽  
Madeleine J. Smith ◽  
Joohyung Lee ◽  
...  
Keyword(s):  
Brain Injury ◽  
Rat Model ◽  
Ischemic Brain Injury ◽  
Behavioral Testing ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury

Systemic G-CSF treatment does not improve long-term outcome after neonatal hypoxic-ischemic brain injury

2010 ◽  
Vol 222 (S 01) ◽  
Author(s):  
GW Schlager ◽  
E Griesmaier ◽  
K Wegleiter ◽  
V Neubauer ◽  
M Urbanek ◽  
...  
Keyword(s):  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury
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