ArticleCNS neuroscience & therapeutics2026
Propofol-Facilitated Recovery Sleep Modulates Cognitive Function via Slow Oscillation-Spindle Coupling After Acute Sleep Deprivation in Rats.
Article in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
backgroundSleep deprivation (SD) is common but underrecognized in intensive care unit (ICU) patients and contributes to delirium and long-term neurocognitive deficits. Propofol is widely used for titratable ICU sedation and has potential neuroprotective effects, but the mechanisms underlying its cognitive benefits during recovery sleep remain unclear. Evidence shows that coupling between slow oscillations (SO) and spindles during sleep is associated with memory consolidation processes. We hypothesized that propofol-facilitated recovery sleep after acute SD would strengthen SO-spindle coupling aligned to the SO up state and thereby improve cognition.
methodsMale Sprague-Dawley rats (8-12 weeks, total n = 67) were assigned to control (CON), SD without intervention (SDN), spontaneous recovery (SDS), or propofol-supported recovery (SDP). All SD groups underwent 48 h of total deprivation. During recovery, SDP received propofol (20 mg·kg
resultsSleep deprivation impaired BM and NOR performance. Propofol during recovery restored spatial performance and 24-h recognition retention. Propofol also increased SO density compared with SDS (11.13 ± 0.14 vs. 9.49 ± 1.26 events/min, p = 0.040) and improved phase-accurate SO-spindle alignment, with higher phase-vector projection (Vproj; 0.30 ± 0.11 vs. -0.33 ± 0.37, p = 0.036), increased up-phase events (0.38 ± 0.01 vs. 0.16 ± 0.10, p = 0.036), and significant up-state preference only in SDP (V-test, p = 0.035). Molecularly, propofol decreased the NKCC1/KCC2 ratio by reducing NKCC1 and increasing KCC2.
conclusionPropofol-facilitated recovery sleep supports spatial and recognition memory, accompanied by up-state-precise SO-spindle coupling and reduced NKCC1/KCC2. These findings suggest SO-spindle alignment may serve as a candidate EEG marker of recovery sleep and highlight chloride-transport-related pathways as therapeutic targets for SD-related cognitive impairment.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.