Dexamethasone inhibits ischemia-induced transient reduction of neurotrophin-3 mRNA in rat hippocampal neurons

被引：13

作者：

Yang, JT

Chang, CN

Lee, TH

Hsu, JC

Lin, TN

Wu, JH ^{[1
]}

机构：

[1] Chang Gung Univ, Coll Med, Mol Genet Lab 3, Tao Yuan 333, Taiwan

[2] Chang Gung Mem Hosp, Dept Neurosurg, Taipei 105, Taiwan

[3] Chang Gung Mem Hosp, Dept Neurol, Taipei 105, Taiwan

[4] Chang Gung Mem Hosp, Dept Anesthesiol, Taipei 105, Taiwan

[5] Acad Sinica, Inst Biomed Sci, Div Neurosci, Taipei 115, Taiwan

来源：

NEUROREPORT | 1998年 / 9卷 / 15期

关键词：

cerebral ischemia; dexamethasone; hippocampus; in situ hybridization; neurotrophin-3;

D O I：

10.1097/00001756-199810260-00026

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

DEXAMETHASONE (DEX) increases the expression of neurotrophin-3 (NT-3) in normal rat hippocampal neurons, whereas transient forebrain ischemia reduces the NT-3 mRNA level. The effect of DEX on the expression of NT-3 mRNA in injured brain cells after ischemia has not been investigated, however. Using in situ hybridization and ribonuclease protection assay methods, we studied NT-3 mRNA expression in rats with and without DEX administration after transient forebrain ischemia. Without DEX treatment, NT-3 mRNA was down-regulated in the hippocampal neurons at 2, 4, 12 h and returned to basal levels 24 h following ischemia. With DEX treatment, however, NT-3 mRNA showed no change at 2, 4 and 12 h and increased 24 h after ischemia. The results indicate that DEX inhibits ischemia-induced NT-3 mRNA down-regulation during the first 12 h and up-regulates NT-3 mRNA 24 h after ischemia. DEX administration might be effective in influencing some of the pathophysiological effects of ischemia in the hippocampus. (C) 1998 Lippincott Williams & Wilkins.

引用

页码：3477 / 3480

页数：4