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Neuropsychopharmacology. 2014 Oct;39(11):2497-505. doi: 10.1038/npp.2014.106. Epub 2014 May 12.

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

Author information

1
Department of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands.
2
Department of Bio-Medical Sciences, Section of Physiology, University of Catania, Catania, Italy.
3
Laboratory of Biological Psychology, Faculty of Psychology and Educational Sciences, University of Leuven, Leuven, Belgium.
4
Department of Neuropsychology and Psychopharmacology, Maastricht University, Maastricht, The Netherlands.

Abstract

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/protein kinase G (PKG) signaling mediates early memory consolidation as well as early-phase LTP, whereas cAMP/protein kinase A (PKA) signaling mediates late consolidation and late-phase-like LTP. In addition, 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.

PMID:
24813825
PMCID:
PMC4207334
DOI:
10.1038/npp.2014.106
[Indexed for MEDLINE]
Free PMC Article

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