The extracellular matrix and diffusion barriers in focal cortical dysplasias
Language English Country France Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Astrocytes metabolism MeSH
- Brevican analysis MeSH
- Diffusion MeSH
- Child MeSH
- Adult MeSH
- Epilepsy MeSH
- Extracellular Matrix chemistry metabolism MeSH
- Extracellular Space chemistry metabolism MeSH
- Iontophoresis methods MeSH
- Middle Aged MeSH
- Humans MeSH
- Malformations of Cortical Development, Group I MeSH
- Malformations of Cortical Development metabolism pathology MeSH
- Adolescent MeSH
- Young Adult MeSH
- Brain Diseases metabolism pathology MeSH
- Neocortex pathology MeSH
- Child, Preschool MeSH
- Tenascin analysis MeSH
- Versicans analysis MeSH
- Check Tag
- Child MeSH
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Adolescent MeSH
- Young Adult MeSH
- Male MeSH
- Child, Preschool MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Brevican MeSH
- tenascin R MeSH Browser
- Tenascin MeSH
- Versicans MeSH
Focal cortical dysplasias (FCDs) of the brain are recognized as a frequent cause of intractable epilepsy. To contribute to the current understanding of the mechanisms of epileptogenesis in FCD, our study provides evidence that not only cellular alterations and synaptic transmission, but also changed diffusion properties of the extracellular space (ECS), induced by modified extracellular matrix (ECM) composition and astrogliosis, might be involved in the generation or spread of seizures in FCD. The composition of the ECM in FCD and non-malformed cortex (in 163 samples from 62 patients) was analyzed immunohistochemically and correlated with the corresponding ECS diffusion parameter values determined with the real-time iontophoretic method in freshly resected cortex (i.e. the ECS volume fraction and the geometrical factor tortuosity, describing the hindrances to diffusion in the ECS). The ECS in FCD was shown to differ from that in non-malformed cortex, mainly by the increased accumulation of certain ECM molecules (tenascin R, tenascin C, and versican) or by their reduced expression (brevican), and by the presence of an increased number of astrocytic processes. The consequent increase of ECS diffusion barriers observed in both FCD type I and II (and, at the same time, the enlargement of the ECS volume in FCD type II) may alter the diffusion of neuroactive substances through the ECS, which mediates one of the important modes of intercellular communication in the brain - extrasynaptic volume transmission. Thus, the changed ECM composition and altered ECS diffusion properties might represent additional factors contributing to epileptogenicity in FCD.
References provided by Crossref.org
ALS-like pathology diminishes swelling of spinal astrocytes in the SOD1 animal model
Astrocytes and extracellular matrix in extrasynaptic volume transmission
