Abstracts

Rationale: It is well known that Status Epilepticus (SE) induces neuronal damage in the developing brain, but its mechanisms are not fully understood. TNFR1 may contribute to seizure-induced neuronal death in the adult hippocampus, but its role in SE-induced damage in the immature brain is unknown. The goal of this study was to evaluate the expression of TNFR1 in a lithium-pilocarpine model of SE in rat pups. Methods: P14 rats were administered intraperitoneally with lithium (3 mEq/kg) and, 20 hours later, SE was induced with subcutaneous pilocarpine (60 mg/kg). The control group received only lithium. Anesthetized animals were perfused with 4% paraformaldehyde and 0.1% picric acid or 4% paraformaldehyde in 0.1 M phosphate-buffer 24 hours after induction of SE. Neuronal injury was evaluated by hematoxilin-eosin (H&E) staining in 10 uM paraffin-embedded sections, whereas the expression of TNFR1 was assessed by light immunohistochemistry in floating sections sectioned to 40 uM. Results: H&E staining showed neuronal damage in hippocampal CA1 and dentate gyrus granule cell layer, mediodorsal thalamic and medial amygdala nuclei following SE, but not in control animals. TNFR1-immunoreactive cells were detected after SE in brain areas displaying injured cells with eosinophilic cytosol and pyknotic nucleus, a morphology suggestive of necrosis. No immunoreactivity was observed in control animals. Conclusions: TNFR1 may be involved in the mechanisms that induce neuronal necrosis in the immature rat brain following SE.