Since consistent findings were reported in similar studies involving resected FCD tissue, glioneuronal tumors and dysembryoplastic neuroepithelial tumors from clinical patients associated with chronic intractable epilepsy which are highly epileptogenic (Aronica et al., 2001, 2003), we can speculate that chronic seizure activity could contribute to the strong expression of mGluR5 in neuronal components in the cortical dysplasia although the role of group I mGluRs is not yet completely understood (Bruno et al., 1999). This evidence concerns the gene GRM5 and cerebral cortical dysplasia.