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Age-related impairment of declarative memory: linking memorization of temporal associations to GluN2B redistribution in dorsal CA1.

Aging cell (2020-10-04)
Alice Shaam Al Abed, Azza Sellami, Mylene Potier, Eva-Gunnel Ducourneau, Pauline Gerbeaud-Lassau, Laurent Brayda-Bruno, Valerie Lamothe, Nathalie Sans, Aline Desmedt, Peter Vanhoutte, Catherine Bennetau-Pelissero, Pierre Trifilieff, Aline Marighetto
ABSTRACT

GluN2B subunits of NMDA receptors have been proposed as a target for treating age-related memory decline. They are indeed considered as crucial for hippocampal synaptic plasticity and hippocampus-dependent memory formation, which are both altered in aging. Because a synaptic enrichment in GluN2B is associated with hippocampal LTP in vitro, a similar mechanism is expected to occur during memory formation. We show instead that a reduction of GluN2B synaptic localization induced by a single-session learning in dorsal CA1 apical dendrites is predictive of efficient memorization of a temporal association. Furthermore, synaptic accumulation of GluN2B, rather than insufficient synaptic localization of these subunits, is causally involved in the age-related impairment of memory. These challenging data identify extra-synaptic redistribution of GluN2B-containing NMDAR induced by learning as a molecular signature of memory formation and indicate that modulating GluN2B synaptic localization might represent a useful therapeutic strategy in cognitive aging.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
β-Estradiol, ≥98%
Sigma-Aldrich
Anti-NR2B Antibody, Upstate®, from rabbit