Temporal binding function of dorsal CA1 is critical for declarative memory formation
Proc Natl Acad Sci USA. 2017-09-05; 114(38): 10262-10267
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Sellami A(1)(2), Al Abed AS(1)(2), Brayda-Bruno L(1)(2), Etchamendy N(1)(2), Valério S(1)(2), Oulé M(1)(2), Pantaléon L(1)(2), Lamothe V(1)(2), Potier M(1)(2), Bernard K(3), Jabourian M(3), Herry C(1)(2), Mons N(2)(4), Piazza PV(1)(2), Eichenbaum H(5), Marighetto A(6)(2).
(1)Neurocentre Magendie, Physiopathologie de la Plasticité Neuronale, U1215, INSERM, F-33000 Bordeaux, France.
(2)Université de Bordeaux, F-33000 Bordeaux, France.
(3)Institut de Recherche Internationale Servier, 92150 Suresnes, France.
(4)Institut de Neurosciences Cognitives et Intégratives d’Aquitaine, UMR 5287, CNRS, F-33600 Pessac, France.
(5)Center for Memory and Brain, Boston University, Boston, MA 02215.
(6)Neurocentre Magendie, Physiopathologie de la Plasticité Neuronale, U1215, INSERM, F-33000 Bordeaux, France; .
Temporal binding, the process that enables association between discontiguous stimuli in memory, and relational organization, a process that enables the flexibility of declarative memories, are both hippocampus-dependent and decline in aging. However, how these two processes are related in supporting declarative memory formation and how they are compromised in age-related memory loss remain hypothetical. We here identify a causal link between these two features of
declarative memory: Temporal binding is a necessary condition for the relational organization of discontiguous events. We demonstrate that the formation of a relational memory is limited by the capability of temporal binding, which depends on dorsal (d)CA1 activity over time intervals and diminishes in aging. Conversely, relational representation is successful even in aged individuals when the demand on temporal binding is minimized, showing that relational/declarative memory per se is not impaired in aging. Thus, bridging temporal intervals by dCA1 activity is a critical foundation of relational representation, and a deterioration of this mechanism is responsible for the age-associated memory impairment.