Abstracts

Thalamic nuclei are mentioned among the structures undergoing histopathological changes in several experimental models of epilepsy in adult rats but there are discrepancies in the description of the distribution of thalamic damage. On the other hand, data about neuronal damage of thalamic nuclei and about dynamics of this process in young animals are only sparse. The aim of this study is to describe the topography and temporal progression of neuronal degeneration after status epilepticus in the thalamus of immature rats.
Status epilepticus (SE) was induced in Wistar albino rat pups 12, 15, 18, 21 or 25 days old (P12-P25) with pilocarpine (40 mg/kg i.p.) after pretreatment with lithium chloride (3 mmol/kg, i.p.). Only animals exhibiting clear-cut motor SE were included in this study. The rats survived for 4, 8, 12, 24, 48 h and/or 1 week after SE. The animals were perfused under an overdose of urethane anestesia with phosphate-buffered saline (PBS) followed by 4 % paraformaldehyde in PBS. Coronal sections (40 [micro]m) were cut on a cryostat, mounted onto gelatine-coated slides, and stained with cresyl violet and with a novel fluorescent stain used for detection of degenerating neurons (Fluoro-Jade B, FJB). Sections were examined with an epifluorescence microscope using FITC filter sets.
Moderate or large number of degenerating neurons was consistently found only in the mediodorsal and in the lateral dorsal and lateral posterior nuclei in P12 rats. In addition to above mentioned changes P15 and P18 rats exhibited a moderate or large number of degenerating neurons also in the paratenial nucleus, in the reuniens nucleus, in the submedius and posterior nuclei and in the ventral nuclei. In older animals (P21 and P25) was neuronal degeneration evident also in other thalamic nuclei namely after longer survival intervals. Degenerating neurons were thus found in the dorsal nucleus of the lateral geniculate body and in several subnuclei of the medial geniculate nucleus.
Presented data provides evidence that pilocarpine[ndash]induced SE causes a substantial neuronal damage not only in the basal telencephalic and limbic structures but also in several functionally heterogenous thalamic nuclei as early as on postnatal day 12 and that these changes were evident in some nuclei from 4 hours up to 1 week after SE.
[Supported by: Grant 309/01/0285 of the Grant Agency of the Czech Republic.]