Radiation-induced long-term alterations in hippocampus under experimental conditions
Language English Country Czech Republic Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
22533885
PII: 37654
Knihovny.cz E-resources
- MeSH
- Ki-67 Antigen analysis MeSH
- Astrocytes pathology MeSH
- Radiation Dosage MeSH
- Glial Fibrillary Acidic Protein analysis MeSH
- Hippocampus metabolism pathology radiation effects MeSH
- Immunohistochemistry MeSH
- Rats MeSH
- Rats, Wistar MeSH
- Gamma Rays 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
- Ki-67 Antigen MeSH
- Glial Fibrillary Acidic Protein MeSH
BACKGROUNDS: The aim of the present study was to investigate the effect of ionizing radiation on the cell population that co-forms hippocampal formation in an adult rat brain. MATERIALS AND METHODS: Adult male Wistar rats were exposed to whole-body irradiation with fractionated doses of gamma rays (the total dose of 4 Gy). Thirty, 60 and 90 days after irradiation the cell-specific types housed in the CA1, CA3 subregions and adjacent layers were labelled using immunohistochemistry for specific cell phenotypes; Ki-67 marker was used for proliferating cells and GFAP for detection of astrocytes. RESULTS: During the 30th day post-exposure, a considerable increase in the numbers of Ki-67-positive cells was seen. Moreover, significant decline in the density of neurons, mostly in the CA1 subregion, was observed on the 60th day. Slight overaccumulation of Ki-67-positive cells was seen in CA1 area 90 days after radiation treatment. Temporary decrease of GFAP-positive astrocytes was seen thirty days after irradiation, followed by their subsequent increase 60 days after exposure. Secondary decrease of GFAP-positive cells in both of regions was found in the group surviving 90 days post-irradiation. CONCLUSION: Results showed that radiation response of neurons and astrocytes that form the adult hippocampus may play contributory role in the development of prognostically unfavourable adverse radiation-induced late effect.