Table 3.
Summary of the modifying effects of inflammation on seizure/Status epilepticus model in the developing brain
| Consequences of seizure‐inducing agents in naïve animals | Consequences of seizure‐inducing agents after an immune challenge | |||
|---|---|---|---|---|
| Seizure occurrence / cell injury | Epileptogenesis | Type of immune challenge | Inflammation‐induced modification | |
| Short Hyperthermic Seizure |
Hypethermia‐induced seizures No cell injury |
No Only for Prolonged HS or HSE |
LPS |
Absence of cell injury Decrease of Sz threshold in adulthood 73. |
| Kainic acid |
Dose dependence on seizure precipitation No cell injury in immature brain |
No Epileptogenesis | LPS |
Increased cell injury in P17 90
Induced hyperthermic seizure with subconvulsant dose of kainate in P14 70 Decreased seizure susceptibility in adulthood |
| Lithium pilocarpine |
P7: Very little P14: CA1 Yes in 10–20% P21: Hilus‐CA3 Yes 57 |
After P7 SE: No After P14 SE: 10–20% SRS After P21 SE: about 100% SRS 57 |
LPS |
Increased SE‐induced cell injury 64
Increased epileptogenesis after SE at P14 81 |
| IL1β |
Increase SE‐induced cell injury (Auvin, unpublished) |
|||
| Rapid Kindling | No |
Epileptogenesis 91, 92, 93 |
LPS | Increased Epileptogenesis without change in hippocampal excitability 81 |
HS, Hyperthermic Seizures; HSE, Hyperthermic Status Epilepticus; IL1β, InterLeukin 1β; LPS, Lipopolysaccharides; P7, 7th postnatal day.