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

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology (2014-05-13)
Eva Bollen, Daniela Puzzo, Kris Rutten, Lucia Privitera, Jochen De Vry, Tim Vanmierlo, Gunter Kenis, Agostino Palmeri, Rudi D'Hooge, Detlef Balschun, Harry M W Steinbusch, Arjan Blokland, Jos Prickaerts
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.

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Rolipram, solid, ≥98% (HPLC)

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