Accepted January 24, 2003.
Expression and Cell Distribution of Group I and Group II Metabotropic Glutamate Receptor Subtypes in Taylor-type Focal Cortical Dysplasia
Article first published online: 9 JUN 2003
Volume 44, Issue 6, pages 785–795, June 2003
How to Cite
Aronica, E., Gorter, J. A., Jansen, G. H., Van Veelen, C. W. M., Van Rijen, P. C., Ramkema, M. and Troost, D. (2003), Expression and Cell Distribution of Group I and Group II Metabotropic Glutamate Receptor Subtypes in Taylor-type Focal Cortical Dysplasia. Epilepsia, 44: 785–795. doi: 10.1046/j.1528-1157.2003.54802.x
- Issue published online: 9 JUN 2003
- Article first published online: 9 JUN 2003
- Metabotropic glutamate receptors;
- Focal cortical dysplasia;
- Balloon cells;
Summary: Purpose: Focal cortical dysplasia (FCD) is known to be a major cause of intractable epilepsy. The cellular mechanism(s) underlying the epileptogenicity of FCD remain largely unknown. Because recent studies indicate that metabotropic glutamate receptor subtypes (mGluRs) play a role in epileptogenesis, we investigated the expression and cellular distribution pattern of mGluRs in FCD specimens.
Methods: Immunocytochemical expression of group I and group II mGluR subtypes was investigated in 15 specimens of human FCD obtained during epilepsy surgery.
Results: Strong mGluR1α and mGluR5 (group I mGluRs) immunoreactivity (IR) was observed in the majority of FCD specimens in dysplastic as well as in heterotopic neurons. mGluR1α was expressed in a subpopulation of neurons (mainly large dysplastic cells), whereas mGluR5 was represented in a higher percentage of dysplastic neuronal cells. Group II mGluRs (mGluR2/3) IR was observed less frequently than that in group I mGluRs and generally appeared in <10% of the dysplastic neurons. IR for all three mGluR subtypes was observed in balloon cells. mGluR2/3 appeared to be most frequently expressed in glial fibrillary acidic protein (GFAP)-positive balloon cells (glial type), and mGluR1α, in microtubule-associated protein (MAP)2-positive cells (neuronal type). mGluR5 was present in the majority of balloon cells. Occasionally glial mGluR1α IR was observed in bizarre glial cells with di- or multinuclei. Reactive astrocytes were intensively stained, mainly with mGluR5 and mGluR2/3.
Conclusions: The cellular distribution of mGluR subtypes, with high expression of mGluR1α and mGluR5 in dysplastic neurons, suggests a possible contribution of group I mGluRs to the intrinsic and high epileptogenicity of dysplastic cortical regions.