The Effect of Transient Global Ischemia on Inositol 1,4,5-Trisphosphate 3-kinase mRNA expression in Gerbil

J Korean Neurol Assoc > Volume 16(6); 1998 > Article

Journal of the Korean Neurological Association 1998;16(6): 872-878.

일과성 전뇌 허혈이 모래쥐 뇌에서 Inositol 1,4,5-trisphosphate 3-kinase 발현에 미치는 영향

고성범, 이대희

고려대학교 의과대학 신경과학교실

The Effect of Transient Global Ischemia on Inositol 1,4,5-Trisphosphate 3-kinase mRNA expression in Gerbil

Seong-beom Koh, Dae-Hie Lee

Department of Neurology, College of Medicine, Korea University

Abstract

Background : Excitotoxicity and perturbation of neuronal Ca2+ homeostasis may play an important role in ischemia-induced neuronal cell injury. The primary emphasis of this study is the effect of transient global ischemia on the metabolism of inositol-1,4,5-triphosphate(IP3), a second messenger that is responsible for mobilization of intracellular Ca2+ stores. This study also investigates the relationship of the ligand-gate glutamate receptor (such as N-methy-D-aspartate receptor) and second messenger system in transient global ischemia. Method : The test animals were divided into two groups : (1) ischemia only group, (2) MK-801 pretreatment and ischemia group. Transient ischemia in Mongolian gerbil was induced by temporary occlusion of common carotid artery for 10 minutes. Expression of c-fos, heat shock protein 72 , IP3 kinase mRNAs were studied with in situ hybridization histochemistry. Result : In ischemia only group, the expression of IP3 kinase was decreased in the ipsilateral side of ischemia. The decrease of IP3 kinase reversed in the MK-801 pretreatment & ischemia group. Conclusions : These results suggest that IP3 may play a role in inducing delayed neuronal death following ischemia. The blocking of early energy failure with NMDA antagonist may protect the IP3 mediated delayed neuronal injury. Key Words : Cerebral Transient Global Ischemia ; IP3 kinase ; in situ hybridization histochemistry ; Gerbil