Abstracts

The aim of our study was to further characterize the capacity of lovastatin to prevent hippocampal neuronal loss after pilocarpine-induced [italic]status epilepticus[/italic] (SE) Adult male Wistar rats were divided into three groups: (A) control rats (n=05), received neither pilocarpine nor lovastatin; (B) rats that received just pilocarpine (n=05); (C) rats that received pilocarpine and lovastatin (n=05). After pilocarpina injection (350mg/kg, i.p.), only rats that displayed continuous, convulsive seizure activity were included in our study. Seizure activity was monitored behaviorally and terminated with an injection of diazepam (10 mg/kg, i.p.) after 4 h of convulsive SE. The rats treated with lovastatin received two doses of 20mg/kg via an oesophagic probe 20 minutes and 24 hours after SE. Seven days after pilocarpine-induced SE, all the animals were perfused and their brains were processed for histological analysis through Nissl and Neo-Timm methods. The cell counts in the Nissl-stained sections performed within the hippocampal formation showed a significant cell loss in rats that received pilocarpine and presented SE (CA1= 27.08 [plusmn] 7.65; CA3= 38.22 [plusmn] 3.98; hilus= 46.02 [plusmn] 1.79) when compared with control group animals (CA1= 53.16 [plusmn] 5.17; CA3= 65.06 [plusmn] 6.18; hilus= 57.8 [plusmn] 5.35). The average neuronal cell number of CA1 subfield of rats that present SE and received lovastatin (52.57 [plusmn] 6.91) was statically significant increased when compared with animals that just presented Lovastatin exert a neuroprotective role in the attenuation of brain damage after SE. (Supported by FAEP, FAPESP, CNPq and CAPES.)