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.
|Titolo:||Improved Long-Term Memory via Enhancing cGMP-PKG Signaling Requires cAMP-PKA Signaling|
|Data di pubblicazione:||2014|
|Citazione:||Improved Long-Term Memory via Enhancing cGMP-PKG Signaling Requires cAMP-PKA Signaling / Bollen, E; Puzzo, Daniela; Rutten, K; Privitera, L; De Vry, J; Vanmierlo, T; Kenis, G; Palmeri, Agostino; D'Hooge, R; Balschun, D; Steinbusch, Hm; Blokland, A; Prickaerts, J.. - In: NEUROPSYCHOPHARMACOLOGY. - ISSN 0893-133X. - 39:11(2014), pp. 2497-2505.|
|Appare nelle tipologie:||1.1 Articolo in rivista|