Arg3.1/Arc mRNA induction by Ca2+ and cAMP requires protein kinase A and mitogen-activated protein kinase/extracellular regulated kinase activation

被引:210
作者
Waltereit, R
Dammermann, B
Wulff, P
Scafidi, J
Staubli, U
Kauselmann, G
Bundman, M
Kuhl, D
机构
[1] Zentrum Mol Neurobiol Hamburg, Inst Neurale Signalverarbeitung, D-20246 Hamburg, Germany
[2] NYU, Ctr Neural Sci, New York, NY 10003 USA
关键词
plasticity; long-term memory; hippocampus; LTP; gene induction; Arg3.1; Arc;
D O I
10.1523/JNEUROSCI.21-15-05484.2001
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Long-term potentiation (LTP) is a cellular model for persistent synaptic plasticity in the mammalian brain. Like several forms of memory, long-lasting LTP requires cAMP-mediated activation of protein kinase A (PKA) and is dependent on gene transcription. Consequently, activity-dependent genes such as c-fos that contain cAMP response elements (CREs) in their 5' regulatory region have been studied intensely. More recently, arg3.1/ arc became of interest, because after synaptic stimulation, arg3.1/arc mRNA is rapidly induced and distributed to dendritic processes and may be locally translated there to facilitate synapse-specific modifications. However, to date nothing is known about the signaling mechanisms involved in the induction of this gene. Here we report that arg3.1/arc is robustly induced with LTP stimulation even at intensities that are not sufficient to activate c-fos expression. Unlike c-fos, the 5' regulatory region of arg3.1/arc does not contain a CRE consensus sequence and arg3.1/arc is unresponsive to cAMP in NIH3T3 and Neuro2a cells. However, in PC12 cells and primary cultures of hippocampal neurons, arg3.1/arc can be induced by cAMP and calcium. This induction requires the activity of PKA and mitogen-activated protein kinase, suggesting a neuron-specific pathway for the activation of arg3.1/arc expression.
引用
收藏
页码:5484 / 5493
页数:10
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