Open AccessAge‐related impairment of declarative memory: linking memorization of temporal associations to GluN2B redistribution in dorsal CA1
Author(s) -
Al Abed Alice Shaam,
Sellami Azza,
Potier Mylene,
Ducourneau EvaGunnel,
GerbeaudLassau Pauline,
BraydaBruno Laurent,
Lamothe Valerie,
Sans Nathalie,
Desmedt Aline,
Vanhoutte Peter,
BennetauPelissero Catherine,
Trifilieff Pierre,
Marighetto Aline
Publication year - 2020
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1111/acel.13243
Subject(s) - nmda receptor , neuroscience , synaptic plasticity , long term potentiation , biology , hippocampal formation , memorization , ampa receptor , glutamate receptor , hippocampus , neuronal memory allocation , psychology , metaplasticity , receptor , cognitive psychology , biochemistry
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.