Abstracts

Rationale: Neonatal hypoxic-ischemic encephalopathy (HIE) is the most common cause of death and disability in human neonates. The reported rate of epilepsy after HIE ranges from 9 to 33% and children with a history of HIE had five times the risk of developing epilepsy when compared with those without HIE. The accurate mechanisms resulted in epilepsy after HIE were noted clearly known. In this study, the role of inflammation on epileptogenesis after neonatal hypoxic-ischemic brain injury would be explored.  Methods: A rat animal model of hypoxic-ischemic (HI)-induced sponatneous epilepsy was established. HI was induced on postnatal day 7 in rat pups by ligating right common carotid artery followed by hypoxia for 2 hours. LPS (0.01mg/kg, Sigma-Aldrich) or vehicle (normal saline) was administered intraperitoneally to pups weakly after carotid artery ligation for 8 weeks. Spontaneous seizures were recorded by continuous electroencephalography (EEG) monitor at 20-21wks of age. Brain histological changes of inflammation, cell damanges, and Mossy fibers were tested. Results: Compared with vehicle group (HIE-V), LPS group (HIE-LPS) increased seizure duration at right hemisphere, the ipsilateral HI damage side (P = 0.001). The seizure duration at left hemisphere was similar in both groups. In addition, HIE-LPS group slightly increased total brain infarct volume but significantly reduced hippocampus infarct volume (P = 0.023). The total cell numbers in right side hippocampus were similar in HIE-V and HIE-LPS groups (Figure 2B). However, HIE-LPS group reduced cell loss at CA1 but exaggerated cell loss at dentate gyrus (DG) of the right side hippocampus when compared to left side hippocampus (P = 0.028). The Timm score in right side hippocampus of HIE-LPS group was significantly higher than HIE-V group (P = 0.028).  Conclusions: LPS-treated HIE rats increased seizure duration and showed enhanced Mossy fibers at ispilateral hippocampus of HI injury compared to vehicle-treated HIE rats.The inflammation plays a role on epileptogeneisis after neonatal HIE. Funding: No funding