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Published on: June 11, 2020
Cognitive Dysfunction and Hippocampal Damage Induced by Hypoxic-Ischemic Brain Injury and Prolonged Febrile
Jung Hye Byeon1, Gun-Ha Kim1, Joo Yeon Kim2
1Department of Pediatrics, Korea University College of Medicine, Seoul, Korea.
Insights
Hypoxic-ischemic encephalopathy (HIE) causes lasting memory and brain damage in developing rats, while prolonged febrile seizures (pFS) alone do not significantly harm the hippocampus.
Area of Science:
- Neuroscience
- Developmental Biology
- Pediatric Neurology
Background:
- Perinatal hypoxic-ischemic encephalopathy (HIE) and prolonged febrile seizures (pFS) are significant childhood neurological conditions.
- The direct impact of pFS on hippocampal injury lacks sufficient experimental evidence.
Purpose of the Study:
- To investigate the individual and combined effects of HIE and pFS on cognitive function and hippocampal histology in a rat model.
- To determine the relative detrimental impact of HIE, pFS, or their combination on brain health.
Main Methods:
- Utilized rat models for HIE (postnatal day 7) and pFS (postnatal day 10).
- Assessed cognitive function via open field tests and the Morris water maze.
- Examined hippocampal pathology, including neuronal damage, astrogliosis, and volume loss, at postnatal week 9.
Main Results:
- HIE induced a seizure-prone state and cognitive decline, evidenced by impaired performance in the Morris water maze.
- Both HIE and combined HIE+pFS groups exhibited significant hippocampal neuronal damage, astrogliosis, and volume loss.
- pFS alone resulted in minimal hippocampal damage without significant cognitive or cellular alterations.
Conclusions:
- pFS in isolation does not appear to cause substantial memory, behavioral, or cellular impairments.
- HIE is a primary driver of persistent memory deficits, neuronal damage, gliosis, and tissue loss in the developing brain.
- Findings enhance understanding of brain development impacts from HIE and pFS.
Objective:
Perinatal hypoxic-ischemic encephalopathy (HIE) and prolonged febrile seizures (pFS) are common neurologic problems that occur during childhood. However, there is insufficient evidence from experimental studies to conclude that pFS directly induces hippocampal injury. We studied cognitive function and histological changes in a rat model and investigated which among pFS, HIE, or a dual pathologic effect is most detrimental to the health of children.
Methods:
A rat model of HIE at postnatal day (PD) 7 and a pFS model at PD10 were used. Behavioral and cognitive functions were investigated by means of weekly open field tests from postnatal week (PW) 3 to PW7, and by daily testing with the Morris water maze test at PW8. Pathological changes in the hippocampus were observed in the control, pFS, HIE, and HIE+pFS groups at PW9.
Results:
The HIE priming group showed a seizure-prone state. The Morris water maze test revealed a decline in cognitive function in the HIE and HIE+pFS groups compared with the pFS and control groups. Additionally, the HIE and HIE+pFS groups showed significant hippocampal neuronal damage, astrogliosis, and volume loss, after maturation. The pFS alone induced minimal hippocampal neuronal damage without astrogliosis or volume loss.
Conclusion:
Our findings suggest that pFS alone causes no considerable memory or behavioral impairment, or cellular change. In contrast, HIE results in lasting memory impairment and neuronal damage, gliosis, and tissue loss. These findings may contribute to the understanding of the developing brain concerning conditions caused by HIE or pFS.
