Daniela Longo

TL;DR: It is proposed that the pilocarpine model can be a valuable tool to investigate the mechanisms involved in TLE, and even more so when standardized to reduce mortality at the time of pilocARPine injection, differences in latent period duration, variability in the lesion extent, and SRS frequency.

TL;DR: It is found that P450scc, the rate-limiting enzyme in steroid synthesis, is upregulated in hippocampal glia during the latent period after pilocarpine-induced SE in rats, suggesting that enhanced steroid synthesis retards epileptogenesis.

TL;DR: The aim was to determine which cells express P450cc and whether neurosteroids play a role in the regulation of epileptogenesis following pilocarpine‐induced status epilepticus (SE).

TL;DR: The presence of hypoxia and cell damage markers in NPY interneurons of rats and patients presenting with recurrent seizures indicates a mechanism of selective vulnerability in a specific neuronal subpopulation, suggesting that interneURons are continuously endangered in rodent and human epileptogenic tissue.

TL;DR: A lesion that destroys the perforant path in CA3 after status epilepticus (SE) induced by pilocarpine injection in 8-week-old rats is described and is characterized by microhemorrhages and ischemia.