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Korean J Crit Care Med > Volume 15(2); 2000 > Article
Korean Journal of Critical Care Medicine 2000;15(2): 75-81.
흰쥐에서 뇌허혈시 해마의 Glutamate Receptor (mGluR5) 변화에 대한 분자생물학적 연구
김해규, 김평주, 백승완, 김인세, 정규섭
부산대학교 의과대학 마취과학교실
Molecular Biologic Study on the Changes of Glutamate Receptor (mGluR5) in Rat Hippocampus after Brain Ischemia
Hae Kyu Kim, Pyong Ju Kim, Seong Wan Baik, Inn Se Kim, Kyoo Sub Chung
Department of Anesthesiology, College of Medicine, Pusan National University, Pusan, Korea.
BACKGROUND: Metabotropic glutamate receptors (mGluRs) participate in the induction of synaptic plasticity phenomena, such as long-term potentiation and long-term depression that are thought to be at the origin of learning and memory. They are also likely to play a role in modulating glutamate-induced neurotoxicity. It will become apparent that mGluRs are excellent targets for the development of drugs that modulate excitatory synaptic transmission. But there were several controversies about the exact role of group 1 mGluRs subtype 5 (mGluR5). This study was designed for evaluation of the neuroprotective role of mGluR5. METHODS: Fifty male Sprague-Dawley rats were divided into three groups, control, MK-801 and lamotrigine. The hippocampus and basal ganglia were removed at 6 hours and 3 days after the one hour transient middle cerebral artery occlusion. The gene expression of mRNA of the brain samples were evaluated by using reverse transcriptase polymerase chain reaction technique. RESULTS: The gene expression of mGluR5 mRNA in hippocampus was increased by 101.96 +/- 18.45% at 6 hours after ischemia and decreased by 50.70 +/- 15.73% at 3 days after ischemia (p<0.01). MK-801 and lamotrigine attenuated the ischemia-induced increases of gene expression of mGluR5 mRNA. In MK-801 group, the expression in basal ganglia was increased by only 0.23 +/- 5.41% at 6 hours after ischemia and decreased by 9.82 +/- 4.35% at 3 days after ischemia. In MK-801 group, the expression in hippocampus was decreased by 3.45 +/- 8.24% and 9.35 5.69% at 6 hours and 3 days after ischemia. In lamotrigine group, the expressions in hippocampus and basal ganglia were decreased by 26.66 +/- 9.85% and 9.45 +/- 5.22% at 6 hours after ischemia. CONCLUSIONS: From these results, the role of mGluR5 was defined as a mediator for neuronal damage after transient focal cerebral ischemia in hippocampus and basal ganglia.
Key Words: Focal brain ischemia; Lamotrigine; Metabotropic glutamate receptor subtype 5 (mGluR5); MK-801; RT-PCR
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