Focal brain injury increases activin beta A mRNA expression in hippocampal neurons

被引:38
作者
Lai, M
Gluckman, P
Dragunow, M
Hughes, PE
机构
[1] UNIV AUCKLAND,SCH MED,RES CTR DEV MED & BIOL,AUCKLAND,NEW ZEALAND
[2] UNIV AUCKLAND,SCH MED,DEPT PHARMACOL,AUCKLAND,NEW ZEALAND
关键词
brain; fos; gene expression; inhibin; NMDA;
D O I
10.1097/00001756-199708180-00011
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The role of activin in the mammalian brain is of increasing interest as evidence accumulates to suggest a number of different neural functions. Here, we report that activin beta A mRNA is transiently induced in dentate gyrus neurons after unilateral mechanical brain injury by saline injection. Expression is dependent on NMDA receptor activation since pretreatment with MK801 (5 mg/kg, i.p.) largely attenuates the signal. Induction also requires de novo protein synthesis, as cycloheximide (10 mg/kg, i.p.) pretreatment abolishes the expression of activin beta A mRNA 1h after injury. These results show that activin beta A mRNA expression is regulated by excitatory activity induced by focal brain injury and suggests a possible neuroplastic role in the recovery from such injury.
引用
收藏
页码:2691 / 2694
页数:4
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