Improved long-term memory via enhancing cGMP-PKG signaling requires cAMP-PKA signaling

E. Bollen, D. Puzzo, K. Rutten, L. Privitera, J. De Vry, T. Vanmierlo, G. Kenis, A. Palmeri, R. D'Hooge, D. Balschun, H.W.M. Steinbusch, A. Blokland, J. Prickaerts*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


Memory consolidation is defined by the stabilization of a memory trace after acquisition, and consists of numerous molecular cascades that mediate synaptic plasticity. Commonly, a distinction is made between an early and a late consolidation phase, in which early refers to the first hours in which labile synaptic changes occur, whereas late consolidation relates to stable and long-lasting synaptic changes induced by de novo protein synthesis. How these phases are linked at a molecular level is not yet clear. Here we studied the interaction of the cyclic nucleotide-mediated pathways during the different phases of memory consolidation in rodents. In addition, the same pathways were studied in a model of neuronal plasticity, long-term potentiation (LTP). We demonstrated that cGMP/PKG signaling mediates early memory consolidation as well as early-phase-LTP, while cAMP/PKA signaling mediates late consolidation and late-phase-like LTP. Additionally, we show for the first time that early-phase cGMP/PKG-signaling requires late-phase cAMP/PKA-signaling in both LTP and long-term memory formation.Neuropsychopharmacology accepted article preview online, 12 May 2014; doi:10.1038/npp.2014.106.
Original languageEnglish
Pages (from-to)2497-2505
Early online date12 May 2014
Publication statusPublished - 12 May 2014

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