TY - JOUR T1 - Arg3.1/Arc mRNA Induction by Ca<sup>2+</sup> and cAMP Requires Protein Kinase A and Mitogen-Activated Protein Kinase/Extracellular Regulated Kinase Activation JF - The Journal of Neuroscience JO - J. Neurosci. SP - 5484 LP - 5493 DO - 10.1523/JNEUROSCI.21-15-05484.2001 VL - 21 IS - 15 AU - Robert Waltereit AU - Björn Dammermann AU - Peer Wulff AU - Joey Scafidi AU - Ursula Staubli AU - Gunther Kauselmann AU - Marsha Bundman AU - Dietmar Kuhl Y1 - 2001/08/01 UR - http://www.jneurosci.org/content/21/15/5484.abstract N2 - 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-fosthat 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-fosexpression. 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. ER -