Expression of Brain-derived Neurotrophic Factor mRNA in Transient Cerebral Ischemic Model of Gerbil Mouse.
- Author:
Min Kyu PARK
1
;
Seung Beom KOH
;
Kun Woo PARK
;
Dae Hie LEE
Author Information
1. Department of Neurology, Korea University, College of Medicine.
- Publication Type:Original Article
- Keywords:
Brain derived neurotrophic factor;
Ischemia;
In situ hybridization;
MK801
- MeSH:
Animals;
Brain;
Brain-Derived Neurotrophic Factor*;
Calcium;
Dentate Gyrus;
Dizocilpine Maleate;
Gerbillinae*;
HSP72 Heat-Shock Proteins;
In Situ Hybridization;
Ischemia;
Mice*;
N-Methylaspartate;
Necrosis;
Peripheral Nervous System;
Prosencephalon;
Reperfusion;
RNA, Messenger*
- From:Journal of the Korean Neurological Association
1998;16(5):689-696
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Brain-derlved neurotrophic factors(BDNF) is critically involved in development and maintenance of the central and peripheral nervous system and the expression of its mRNA increases after various insults such as ischemia. If one takes the protective role of BDNF into consideration, it would be important to understand the mechanism of induction in BDNF mRNA. Although previous reports suggested the relationship between activation of N-methy]-D-aspartate(NMDA) receptor and induction of BDNF mRNA following ischemic insult, the mechanism is not clearly understood. METHODS: In this experiment, in situ hybridization was used to study expression of mRNA for c-fos, heat shock protein 72, and brain-derived neurotrophic factor in the gerbil brain after 15 minutes of forebrain ischemia as well as with MK801 pretreatment before ischemia. RESULTS: Transient ischemic insult caused the induction of c-fos and heat shock protein 72 mRNA expression which partially blocked by MK801 within 24 hours after reperfusion. From 30 minutes to 4 hours after the reperfusion, the level of brain-derived neurotrophic factor mRNA was increased in the granule cells of the dentate gyrus. In addition, the increase of BDNF mRNA was not influenced by NMDA receptor antagonist, MK801. CONCLUSIONS: The expression of BDNF mRNA after acute ischemia could be induced not by NMDA receptor related intracellular calcium change, but by some other factors which requires further effort to be solved. Finally, if the changes of mRNA expression lead to alterations in the relative availability of BDNF, this might influence functional outcome and necrosis following ischemia.
