Abstracts

Rationale: Aim of this study is to describe distribution of status epilepticus-induced early neuronal degeneration in the cortical (neocortex, hippocampal formation, piriform cortex) and subcortical structures (basal ganglia, thalamus) in 12 - and 25-day-old rats surviving 4 h after SE was interrupted. Methods: Lithium-pilocarpine model of status epilepticus (SE) was elicited in 12- and 25-day-old Wistar rats. Lithium chloride (3mmol/kg, i.p.) was injected 24 hours before pilocarpine (40 mg/kg i.p.). Only animals exhibiting convulsive SE were included in this study. The rats survived for 4 h after SE; then they were perfused with phosphate-buffered saline (PBS) followed by 4 % paraformaldehyde in PBS under an overdose of urethane anesthesia. Coronal sections (40 μm thick) were cut on a kryostat and processed with cresyl violet or with a fluorescent stain Fluoro-Jade B (FJB) used for detection of degenerated neurons. Results: P12 rats: A small to moderate number of FJB-positive neurons was found in the medial prefrontal and cingular cortex. Degenerated neurons were evident only in the dentate gyrus on the hippocampalformation; negative finding was in the pyriform cortex. In the subcortical structures FJB-positive neurons were found in the amygdala (cortical and medial nuclei), in the ventral claustrum (DEN) and in several thalamic nuclei (MD, LD, Re). In other cortical areas and subcortical structures no FJB-positive cells were found. P25 rats: The number of FJB-positive neurons was significantly higher than in P12 rats. Moderate to massive neuronal degeneration was found in medial prefrontal, cingular, insular and perirhinal cortical areas. The hippocampus and piriform cortex exhibited only a few FJB-positive neurons. Massive degeneration was demonstrated in the accumbens nucleus (shell), in the ventral claustrum (DEN) and in several amygdala nuclei. Majoritiy of FJB-positive neurons in the thalamus was localized in the MD, LD, LP, Re and in the reticular thalamic nucleus. Conclusions: The age of animals at the time of SE determined the severity of neuronal damage. In P12 rats degenerated neurons were evident only in the medial prefrontal cortex, in the amygdala, in the ventral claustrum and in the thalamus. In P25 rats, the number of degenerated neurons increased and moderate to masive neuronal damage occured in the medial prefrontal cortex, in the insular and perirhinal cortical areas, in the several amygdalar nuclei, in the ventral striatum and claustrum and in the thalamus. The density of degenerated neurons in the hipopocampus was low in both age groups. Supported by grant No.304/07/1137 of the Grant Agency of the Czech Republic.