Status Epilepticus Causes Necrotic Damage in the Mediodorsal Nucleus of the Thalamus in Immature Rats

Status Epilepticus Causes Necrotic Damage in the Mediodorsal Nucleus of the Thalamus in Immature Rats

Status epilepticus (StE) in immature rats causes long-term functional impairment. Whether this is associated with structural alterations remains controversial. The present study was designed to test the hypothesis that StE at an early age results in neuronal loss. StE was induced with lithium-piloca...

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Bibliographic Details
Published in:The Journal of neuroscience Vol. 21; no. 10; pp. 3593 - 3599
Main Authors: Kubova, Hana, Druga, Rastislav, Lukasiuk, Katarzyna, Suchomelova, Lucie, Haugvicova, Renata, Jirmanova, Iza, Pitkanen, Asla
Format: Journal Article
Language:English
Published: United States Soc Neuroscience 15-05-2001
Society for Neuroscience
Subjects:
Animals
Antigens, CD
Antigens, Neoplasm
Antigens, Surface - metabolism
Apoptosis
Avian Proteins
Basigin
Blood Proteins
Caspase 3
Caspases - metabolism
Cytochrome c Group - metabolism
Disease Models, Animal
Disease Progression
Immunohistochemistry
In Situ Nick-End Labeling
Lithium Chloride
Male
Mediodorsal Thalamic Nucleus - metabolism
Mediodorsal Thalamic Nucleus - pathology
Membrane Glycoproteins - metabolism
Microglia - metabolism
Microglia - pathology
Microscopy, Electron
Necrosis
Neurons - metabolism
Neurons - pathology
Pilocarpine
Rats
Rats, Wistar
Status Epilepticus - chemically induced
Status Epilepticus - pathology
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Summary:Status epilepticus (StE) in immature rats causes long-term functional impairment. Whether this is associated with structural alterations remains controversial. The present study was designed to test the hypothesis that StE at an early age results in neuronal loss. StE was induced with lithium-pilocarpine in 12-d-old rats, and the presence of neuronal damage was investigated in the brain from 12 hr up to 1 week later using silver and Fluoro-Jade B staining techniques. Analysis of the sections indicated consistent neuronal damage in the central and lateral segments of the mediodorsal nucleus of the thalamus, which was confirmed using adjacent cresyl violet-stained preparations. The mechanism of thalamic damage (necrosis vs apoptosis) was investigated further using TUNEL, immunohistochemistry for caspase-3 and cytochrome c, and electron microscopy. Activated microglia were detected using OX-42 immunohistochemistry. The presence of silver and Fluoro-Jade B-positive degenerating neurons in the mediodorsal thalamic nucleus was associated with the appearance of OX-42-immunopositive activated microglia but not with the expression of markers of programmed cell death, caspase-3, or cytochrome c. Electron microscopy revealed necrosis of the ultrastructure of damaged neurons, providing further evidence that the mechanism of StE-induced damage in the mediodorsal thalamic nucleus at postnatal day 12 is necrosis rather than apoptosis. Finally, these data together with previously described functions of the medial and lateral segments of the mediodorsal thalamic nucleus suggest that some functions, such as adaptation to novelty, might become compromised after StE early in development.
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ISSN:0270-6474
1529-2401
1529-2401
DOI:10.1523/jneurosci.21-10-03593.2001