Upregulation of Glutamate Receptors in Rat Cerebral Cortex with Neuronal Migration Disorders.
10.3346/jkms.2004.19.3.419
- Author:
Min Cheol LEE
1
;
Jae Jin SHIM
;
Jae Hyoo KIM
;
Myeong Kyu KIM
;
Young Jong WOO
;
Woong Ki CHUNG
;
Jung Jin SUH
;
Sang Chae NAM
;
Ji Shin LEE
;
Yeong Seon KIM
;
Jin Hee KIM
;
Hyoung Ihl KIM
Author Information
1. Department of Pathology, Chonnam National University Medical School, Gwangju, Korea. mclee@jnu.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Cerebral Cortex, Cortical Dysplasia;
Epilepsy;
Neuron;
Neuronal Migration Disorder (NMD);
Radiation;
Receptors, Glutamate
- MeSH:
Animals;
Cell Movement;
Cerebral Cortex/*metabolism;
Electroencephalography;
Glutamic Acid/metabolism;
Immunohistochemistry;
Kainic Acid/pharmacology;
Neurons/*metabolism/pathology;
Rats;
Rats, Wistar;
Receptors, Glutamate/metabolism;
Receptors, N-Methyl-D-Aspartate/*biosynthesis;
Support, Non-U.S. Gov't;
Time Factors;
*Up-Regulation
- From:Journal of Korean Medical Science
2004;19(3):419-425
- CountryRepublic of Korea
- Language:English
-
Abstract:
Neuronal migration disorders (NMDs) constitute the main pathologic substrate of medically intractable epilepsy in human. This study is designed to investigate the changes in expression of glutamate receptor subtypes on radiation-induced NMD in rats. The lesion was produced by intrauterine irradiation (240 cGy) on E17 rats, and then 10 weeks old rats were used for the study. The pathologic and immunohistochemical findings for glutamate receptor subunit proteins on NMD cortex were correlated with development of behavioral seizures and EEG abnormality. Spontaneous seizures uncommonly occurred in NMD rats (5%); however, clinical stages of seizures were significantly increased in NMD rats by an administration of kainic acid. Brains taken from irradiated rats revealed gross and histopathologic features of NMD. Focal cortical dysplasia was identified by histopathology and immunohistochemistry with neurofilament protein (NF-M/H). Significantly strong NR1 and NR2A/B immunoreactivities were demonstrated in cytomegalic and heterotopic neurons of NMD rats. The results of the present study indicate that epileptogenesis of NMD might be caused by upregulation of glutamate receptor expression in dysplastic neurons of the rat cerebral cortex with NMDs.
