Premium
Nitric oxide synthase and NMDA receptor expressions in cavernoma tissues with epileptogenesis
Author(s) -
Kamida T.,
Takeda Y.,
Fujiki M.,
Abe T.,
Abe E.,
Kobayashi H.
Publication year - 2007
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.2007.00885.x
Subject(s) - epileptogenesis , nmda receptor , nitric oxide synthase , glutamate receptor , nitric oxide , immunohistochemistry , hemosiderin , epilepsy , gene isoform , downregulation and upregulation , biology , neuroscience , receptor , chemistry , microbiology and biotechnology , endocrinology , medicine , biochemistry , immunology , gene
Objectives – To investigate the contribution of nitric oxide (NO) and the glutamate systems to epileptogenicity of cavernoma (CA). Methods – Using immunohistochemistry we examined NO synthases (NOS; neuronal, inducible and endothelial) and N ‐methyl‐D‐aspartate (NMDA) receptor subunits 1(NR1) and 2A/B (NR2A/B) in tissues, with and without hemosiderin deposits, adjacent to CA resected from temporal (seven patients) and frontal (one patient) lobes. Results – All isoforms of NOS, especially iNOS expression, was significantly upregulated in company with NR2A/B expression, not only in declining neuronal cells but also in reactive astrocytes in the tissue, with hemosiderin deposits, adjacent to CA and moreover the degree of iNOS expression was significantly correlated with seizure frequency. Conclusions – These preliminary results sustain a speculation that excessive NO may generate in the tissue surrounding CA with repeated microhaemorrhaging and seizures. The neuronal loss and reactive glial proliferation induced by iron or NO may play a role in epileptogenesis.