Abstracts

Rationale: Growing evidence shows that inflammation can contribute to status epilepticus (SE)-induced neuronal injury in the immature brain. Interleukin-1? (IL-1?) gene and protein expression is up regulated following seizures and this cytokine has been associated with neuronal cell death following epileptic activity. The goal of this study was to determine the brain expression of IL-1? in the lithium-pilocarpine model of SE in fourteen-days-old (P14) rat pups.Methods: Rats were given 3 mEq/kg lithium chloride i.p. on the day before the induction of SE, which was carried out at P14 by subcutaneous injection of 100 mg/kg pilocarpine hydrochloride; control animals were given an equal volume of saline subcutaneously. Six (n=5) or 24 h (n=3) following SE rats were anesthetized and transcardially perfused with 4% phosphate-buffered paraformaldehyde; control rats (n=6) were processed similarly. Subsequently, brains were dehydrated, embedded in paraffin and cut into 10-?m-thick coronal sections at the level of dorsal hippocampus. IL-1? was detected by immunohistochemical procedures, whereas Fluoro-Jade B staining was carried out in parallel sections in order to detect neuronal cell death. Results: IL-1? immunoreactivity was not detected in control animals; however, this cytokine was strongly expressed in cells from the CA1 pyramidal layer and in microglia-like cells from the hilus and the dorsomedial thalamic nucleus 6 h after SE onset. This effect disappeared 24 h following seizures, even when injured cells where evidently detected in hippocampus and thalamus. Conclusions: Results suggest that early expression of IL-1? could be associated with SE-induced neuronal cell death mechanisms in the developing rat brain. Supported by CONACYT (grant 106402 to MLLM and scholarship 249772 to DMAC) and PROMEP-SEP (grant PROMEP/103.5/10/5006, PTC-474 to MLLM).