The reaction of the subependymal layer of lateral brain ventricles to striatal ibotenic acid lesions in a long-term study
Language English Country Germany Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
12553706
DOI
10.1078/0065-1281-00663
PII: S0065-1281(04)70142-7
Knihovny.cz E-resources
- MeSH
- 2',3'-Cyclic-Nucleotide Phosphodiesterases analysis MeSH
- Excitatory Amino Acid Agonists toxicity MeSH
- Ki-67 Antigen analysis MeSH
- Astrocytes chemistry drug effects pathology MeSH
- Bromodeoxyuridine analysis MeSH
- Ependyma chemistry drug effects pathology MeSH
- Glial Fibrillary Acidic Protein analysis MeSH
- Immunohistochemistry MeSH
- Rats MeSH
- Ibotenic Acid toxicity MeSH
- Oligodendroglia chemistry drug effects pathology MeSH
- Rats, Long-Evans MeSH
- Proliferating Cell Nuclear Antigen analysis MeSH
- Lateral Ventricles chemistry drug effects pathology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- 2',3'-Cyclic-Nucleotide Phosphodiesterases MeSH
- Excitatory Amino Acid Agonists MeSH
- Ki-67 Antigen MeSH
- Bromodeoxyuridine MeSH
- Glial Fibrillary Acidic Protein MeSH
- Ibotenic Acid MeSH
- Proliferating Cell Nuclear Antigen MeSH
The proliferative activity in the subependymal layer of lateral brain ventricles in adulthood is known. We were interested in the reaction of this layer to ibotenic acid lesions, which simulate neurodegenerative processes in Huntington's disease. Animals with a unilateral ibotenic acid lesion were compared with sham-lesioned animals and control animals with intact brains at 5 and 13 weeks after surgery. Five weeks after surgery, increased proliferation was found in most GFAP-positive astrocytes and to a lesser extent in CNPase-positive oligodendrocytes in comparison with controls. Interestingly, a slight increase in proliferation was found as well in the contralateral non-lesioned hemispheres. Moderate elevation of cell proliferation was found after induction of sham-lesions as well. The intensity of the reaction in the subependymal layer decreased in the following 8 weeks. Only a few scattered cells that originated from the subependymal layer had migrated over a short distance to adjacent brain tissue. We conclude that the reaction of the subependymal layer is (a) non-specific, as it is a response to any type of lesion, and (b) slowly decreases in time.
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