Abstract:
BACKGROUND:Identifying the underlying cellular mechanisms of episodic memory is an important challenge, since this memory, based on temporal and contextual associations among events, undergoes preferential degradation in aging and various neuropsychiatric disorders. Memory storage of temporal and contextual associations is known to rely on hippocampal N-methyl-D-aspartate receptor (NMDAR)-dependent synaptic plasticity, which depends ex vivo on dynamic organization of surface NMDARs. Whether NMDAR surface trafficking sustains the formation of associative memory, however, remains unknown. METHODS:We tested this hypothesis, using single nanoparticle imaging, electrophysiology, and behavioral approaches, in hippocampal networks challenged with a potent modulator of NMDAR-dependent synaptic plasticity and memory, 17β-estradiol (E2). RESULTS:We demonstrate that E2 modulates NMDAR surface trafficking, a necessary condition for E2-induced potentiation at hippocampal cornu ammonis 1 synapses. Strikingly, cornu ammonis 1 NMDAR surface trafficking controls basal and E2-enhanced mnemonic retention of temporal, but not contextual, associations. CONCLUSIONS:NMDAR surface trafficking and its modulation by the sex hormone E2 is a cellular mechanism critical for a major component of episodic memory, opening a new and noncanonical research avenue in the physiopathology of cognition.
journal_name
Biol Psychiatryjournal_title
Biological psychiatryauthors
Potier M,Georges F,Brayda-Bruno L,Ladépêche L,Lamothe V,Al Abed AS,Groc L,Marighetto Adoi
10.1016/j.biopsych.2015.07.017subject
Has Abstractpub_date
2016-05-01 00:00:00pages
735-745issue
9eissn
0006-3223issn
1873-2402pii
S0006-3223(15)00611-3journal_volume
79pub_type
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