Sleep-dependent declarative memory consolidation--unaffected after blocking NMDA or AMPA receptors but enhanced by NMDA coagonist D-cycloserine.
Level 2 - randomized trial
Individual randomized double-blind crossover trials in humans
PubMed 23887151 · doi:10.1038/npp.2013.179
What was done
Across three double-blind, placebo-controlled, crossover studies, human participants learned a declarative word-pair association task prior to sleeping in a laboratory. During retention sleep, participants received pharmacological modulators of glutamatergic neurotransmission: the NMDA receptor blocker ketamine (study 1), the AMPA receptor blocker caroverine (study 2), or the NMDA receptor coagonist D-cycloserine (DCS; study 3). Study 3 also assessed a procedural control task (finger sequence tapping) and tested DCS administration during a wake interval on word-pair retention and number encoding.
What was found
No quantitative values or sample sizes were reported in the abstract. Directionally: - Neither ketamine (NMDA blocker) nor caroverine (AMPA blocker) during retention sleep impaired declarative memory consolidation relative to placebo. - DCS (NMDA coagonist) administered during sleep facilitated consolidation of declarative word pairs, but did not affect procedural finger tapping consolidation. - DCS administered during wakefulness did not alter word-pair retention, but improved number encoding.
Why it matters
This study provides evidence in humans that sleep-dependent declarative memory consolidation relies on NMDA-related synaptic plasticity, demonstrating distinct neurochemical requirements for consolidation during sleep compared with daytime encoding.
Limits
The abstract omits sample size, participant demographics, drug dosages, timing of administration, and quantitative statistics (effect sizes, p-values, or variance). Unmeasured effects on sleep architecture are not detailed.
Cited by
- contradicts Sleep typically produces an approximate 20% improvement in declarative memory retention compared to lack of sleep or NMDA receptor blockade.