Abstracts

Rationale: The amygdala is a prominent telencephalic structure involved in recognition of emotions in sensory signals. Clinical studies have provided evidence that amygdala may be damaged in children or adults with temporal lobe epilepsy (TLE) or following status epilepticus (SE). Several clinical and experimental studies reported atrophy, metabolic changes and neuronal degeneration in the amygdalar complex but systematic study and developmental data about neuronal damage and temporal profile of neuronal degeneration of the amygdala after SE in immature rats are missing.Methods: Lithium-pilocarpine model of SE was elicited in Wistar rat pups 12, 15, 18, 21 and 25 days old. Lithium chloride (3mmol/kg,i.p.) was injected 24 hours before pilocarpine (40 mg/kg i.p.). Only animals exhibiting convulsive status epilepticus (SE) were included in this study. The rats survived for 4, 8, 12, 24, 48 hours or 1 week after SE. The animals were perfused with PBS followed by 4% paraformaldehyde in PBS under an overdose of urethane anesthesia. Coronal sections (40 ?m thick) were cut on a cryostat and processed with cresyl violet or with a fluorescent stain Fluoro - Jade B (FJB) used for detection of degenerated neurons. Sections were examined with an epifluorescence microscope using a filter system suitable for visualizing fluorescein or FITC. Labelled cells were plotted and transferred to standard stereotaxic sections (Paxinos and Watson 2007).Results: A small to moderate number of FJB- positive neurons was found in P12 and P15 old animals. Moderate number of degenerated neurons was observed in medial nucleus and in basomedial nucleus. Since P18 the number of degenerated neurons in these nuclei increased and neuronal degeneration was evident also in central, cortical and lateral nuclei. Massive neuronal degeneration was consistently found in medial nucleus and in the both subdivisions of the basomedial nucleus. In P15 and older rats neuronal damage was found in all survival intervals and its peak was reached at 24 and 48 h after SE. One week after SE number of degenerated neurons was reduced but neuronal degeneration persisted in the majority of the above mentioned amygdalar nuclei.Conclusions: Lithium pilocarpine model of SE resulted in degeneration of neurons in the anygdala in immature rats. Damage was present in P12 group but was much more marked in P18 and older rats and increased with survival interval with a peak at 24 and 48 h after SE. At all survival intervals degenerated neurons significantly prevailed in the medial nucleus and in the subdivisions of the basomedial nucleus. Supported by grants No. 304/07/1137 and P302/10/0971 of the Grant Agency of the Czech Republic and project LC554 of the Ministry of Education of the Czech Republic.