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Updated: Jul 12, 2026
A Ferret Model of Inflammation-sensitized Late Preterm Hypoxic-ischemic Brain Injury
Published on: November 19, 2019
Inflammation contributes to seizure-induced hippocampal injury in the neonatal rat brain
R Sankar1, S Auvin, A Mazarati
1'Division of Neurology, Department of Pediatrics, David Geffen School of Medicine at UCLA, Mattel Children's Hospital at UCLA, Los Angeles, CA 90095, USA. rsankar@ucla.edu
Insights
Pre-existing inflammation exacerbates hippocampal injury in neonatal rat pups during experimental seizures. This highlights inflammation
Area of Science:
- Neuroscience
- Developmental Neuroscience
- Inflammation Research
Background:
- Neuronal injury in the hippocampus from experimental status epilepticus (SE) is age-dependent.
- Neonatal seizures often occur with inflammation, but its role in injury is unclear.
Purpose of the Study:
- To investigate the role of pre-existing inflammation in mediating seizure-induced hippocampal neuronal injury in neonatal rats.
Main Methods:
- Postnatal day 7 and 14 rat pups received lipopolysaccharide (LPS) 2 hours before lithium-pilocarpine-induced status epilepticus (LiPC-SE).
- Histologic methods were used to assess neuronal injury.
Main Results:
- Lipopolysaccharide (LPS) alone did not cause cell injury.
- LPS treatment significantly worsened hippocampal damage induced by LiPC-SE.
- The exacerbation of injury was specific to the CA1 subfield of the hippocampus.
Conclusions:
- Inflammation significantly increases the immature hippocampus's vulnerability to seizure-induced neuronal injury.
- Combined inflammation and seizures in early life may affect long-term outcomes of neonatal seizures.
Objective:
The extent of neuronal injury in the hippocampus produced by experimental status epilepticus (SE) is age dependent and is not readily demonstrable in many models of neonatal seizures. Neonatal seizures often occur in clinical settings that include an inflammatory component. We examined the potential contributory role of pre-existing inflammation as an important variable in mediating neuronal injury.
Materials And Methods:
Postnatal day 7 (P7) and P14 rat pups were injected with lipopolysaccharide (LPS), 2 h prior to SE induced by lithium-pilocarpine (LiPC). Neuronal injury was assessed by well-described histologic methods.
Results:
While LPS by itself did not produce any discernible cell injury at either age, this treatment exacerbated hippocampal damage induced by LiPC-SE. The effect was highly selective for the CA1 subfield.
Conclusions:
Inflammation can contribute substantially to the vulnerability of immature hippocampus to seizure-induced neuronal injury. The combined effects of inflammation and prolonged seizures in early life may impact long-term outcomes of neonatal seizures.
