Dynamic changes of status epilepticus-induced neuronal degeneration in the mediodorsal nucleus of the thalamus during postnatal development of the rat
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
12121296
DOI
10.1046/j.1528-1157.43.s.5.36.x
PII: epis6035
Knihovny.cz E-resources
- MeSH
- Staining and Labeling MeSH
- Nerve Degeneration pathology MeSH
- Fluoresceins MeSH
- Fluorescent Dyes MeSH
- Rats MeSH
- Nissl Bodies pathology MeSH
- Animals, Newborn growth & development MeSH
- Mediodorsal Thalamic Nucleus pathology MeSH
- Organic Chemicals MeSH
- Rats, Wistar MeSH
- Aging physiology MeSH
- Status Epilepticus pathology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Fluoresceins MeSH
- Fluorescent Dyes MeSH
- fluoro jade MeSH Browser
- Organic Chemicals MeSH
PURPOSE: Status epilepticus (SE) was previously found to induce damage in the mediodorsal nucleus of the thalamus (MD) in both adult and immature rats. This study was designed to describe age-related changes of SE-induced neuronal degeneration in this part of the brain. METHODS: SE was induced by LiCl/pilocarpine in five age groups of rats (P12-P25). Distribution of degenerating neurons was studied at various time intervals from 4 h up to 1 week using Fluoro Jade B (FJB) staining. For P12 and P25 rats, an interval of 3 months was added. RESULTS: Damaged neurons were found in all age groups during a 1-week period after SE. Patterns of neuronal degeneration, however, changed in an age-related manner. In animals at P12 and P15, FJB-labeled neurons were located in the central and lateral segment of the MD. In the P18 group, degenerating neurons occurred in all three segments of the MD, with a prevalence in central and lateral subdivisions. In contrast, in P21 and P25 rats, FJB-labeled neurons were predominantly located in the central and medial segments. Degenerating neurons were still present 3 months after SE in the medial segment in P25 animals, whereas no labeled neurons were detected in the P12 group at this time. CONCLUSIONS: Our data demonstrate that the pattern of neuronal degeneration in MD is mainly related to age at SE onset. In addition to damage occurring during the acute phase of SE, a population of degenerating neurons was detected in P25 animals during the chronic period 3 months after SE.
References provided by Crossref.org
Epilepsy Research in the Institute of Physiology of the Czech Academy of Sciences in Prague
