Status epilepticus causes necrotic damage in the mediodorsal nucleus of the thalamus in immature rats
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
11331388
PubMed Central
PMC6762492
DOI
10.1523/jneurosci.21-10-03593.2001
PII: 21/10/3593
Knihovny.cz E-zdroje
- MeSH
- antigeny nádorové * MeSH
- antigeny povrchové metabolismus MeSH
- apoptóza MeSH
- basigin MeSH
- CD antigeny * MeSH
- chlorid lithný MeSH
- cytochromy skupiny c metabolismus MeSH
- elektronová mikroskopie MeSH
- imunohistochemie MeSH
- kaspasa 3 MeSH
- kaspasy metabolismus MeSH
- koncové značení zlomů DNA in situ MeSH
- krevní proteiny * MeSH
- krysa rodu Rattus MeSH
- membránové glykoproteiny metabolismus MeSH
- mikroglie metabolismus patologie MeSH
- modely nemocí na zvířatech MeSH
- nekróza MeSH
- neurony metabolismus patologie MeSH
- nucleus medialis dorsalis thalami metabolismus patologie MeSH
- pilokarpin MeSH
- potkani Wistar MeSH
- progrese nemoci MeSH
- ptačí proteiny * MeSH
- status epilepticus chemicky indukované patologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- antigeny nádorové * MeSH
- antigeny povrchové MeSH
- basigin MeSH
- Bsg protein, Gallus gallus MeSH Prohlížeč
- Bsg protein, rat MeSH Prohlížeč
- Casp3 protein, rat MeSH Prohlížeč
- CD antigeny * MeSH
- chlorid lithný MeSH
- cytochromy skupiny c MeSH
- kaspasa 3 MeSH
- kaspasy MeSH
- krevní proteiny * MeSH
- membránové glykoproteiny MeSH
- pilokarpin MeSH
- ptačí proteiny * MeSH
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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