Glutamate Receptor Subunits Gene Expression in Kainate-induced Temporal Lobe Epilpsy Model.
- Author:
Myeong Kyu KIM
1
;
Sung Min CHOI
;
Seung Han LEE
;
Byeong Chae KIM
;
Ki Hyun CHO
;
Sang Chae NAM
;
Min Chul LEE
Author Information
1. Department of Neurology,Chonnam National University Medical School.
- Publication Type:Original Article
- Keywords:
Temporal lobe epilepsy;
Hippocampal sclerosis;
SE;
NMDA;
AMPA;
Kainic acid
- MeSH:
alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid;
Animals;
D-Aspartic Acid;
Dizocilpine Maleate;
Epilepsy, Temporal Lobe;
Gene Expression*;
Glutamic Acid*;
Hippocampus;
In Situ Hybridization;
Kainic Acid;
N-Methylaspartate;
Neurons;
Rats;
Rats, Sprague-Dawley;
Receptors, Glutamate*;
RNA, Messenger;
Sclerosis;
Seizures;
Temporal Lobe*
- From:Journal of the Korean Neurological Association
2001;19(1):36-44
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: There is considerable controversy about the exact molecular mechanisms of excitatory amino acid receptors in epileptogenesis. METHODS: We used in situ hybridization to examine the hybridization density (HD) of n-methyl- D-aspartic acid receptor type 1 (NMDAR-1) and alpha-amino-3-hydroxy -5-methyl-4-isoxazole-propionate (AMPA) receptor type 2 (GluR-2) mRNA, in the hippocampus obtained from the kainic acid (KA)-induced status epilep-ticus (SE) model. Some Sprague-Dawley rats were injected with KA (10 mg/Kg; I.p.), and others with MK-801 (4 mg/kg) 20 minutes prior to KA. The rats were allowed to have 4-hour SE and were killed at 8 hours or 4 weeks after KA or MK-801/KA injection. HD of NMDAR-1 and GluR-2 mRNA in subfields of the hippocampus was measured by an image analysis system. RESULTS: A typical neuropathological finding of hippocampal sclerosis and spontaneous repetitive seizures (SRS) were observed in the KA injected rats, but not in the MK-801 pretreated rats, killed at 4 weeks. Compared with controls, the rats killed at 8 hours after KA showed increased CA1, CA2, and CA3 NMDAR-1 HD, and stratum granulosum (SG) GluR-2 HD. The increase of NMDAR-1, not GluR-2, HD was blocked effectively by MK-801. The increase of SG GluR-2 HD remained until 4 weeks after the KA injection. CONCLUSIONS: Not only the NMDAR-1activa-tionbut also the GluR-2 activation is an important factor in delaying hippocampal neuronal loss and epileptogenesis. (J Korean Neurol Assoc 19(1):36~44, 2001
