Ischemia in neonatal rats with periventricular leukomalacia and long-term neurobehavioral changes.docVIP

 PAGE \* MERGEFORMAT 13 Ischemia in neonatal rats with periventricular leukomalacia and long-term neurobehavioral changes Of: Hu Yan, JIANG Li, Zhang Min, Qiao Lixing [Abstract] Objective: To establish a rat model of white matter damage, white matter injury of oligodendrocytes (OL) apoptosis and long-term neurobehavioral changes. Methods: Neonatal rats were randomly divided into 5 experimental groups and the control group, making animal models of ischemic white matter damage, observed at different time points after growth and development, HE staining, immunofluorescence labeling observed pathological changes in brain tissue, cell changes, suspension test, open field test, refusal to test the capture reaction neural behavior change. Results: The growth was slower than the control group, HE staining periventricular leukoaraiosis, lateral ventricle increases, myelin phospholipid protein (MBP) immunofluorescence positive cells in the experimental group than in the control group significantly decreased ( P lt;0.05), nervous behavior detection capacity in experimental group decreased nerve. Conclusion: The establishment of white matter damage in neonatal rats 5 days old model is white matter damage in neonatal rats showed white matter oligodendrocyte injury based lesions. [Keywords:] ischemic brain injury, periventricular leukomalacia, oligodendrocyte; neonatal rats Obstetric and neonatal intensive care treatment and technology, greatly improved the survival rate of premature children, but the ensuing brain damage in preterm children is also more prominent. Some studies that brain damage in preterm children, mainly in white matter, periventricular leukomalacia (periventricular leucumalacia, PVL) in preterm children is the main form of brain damage [1], high 24 to 32 weeks in gestational age in preterm children, the occurrence rate of 26% ~ 60% [2]. PVL can cause parts of white matter oligodendrocytes glial cells (oligodendrocyte, OL) damage and loss of pr