ArticleNature and science of sleep2025
Dexmedetomidine Alleviates Hippocampal Tissue Damage in Rapid Eye Movement Sleep-Deprived Rats by Activating BDNF/TrkB Signaling Pathway.
Article in Nature and science of sleep, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- 'Molecular and Cellular Neuroscience': Impacts of Eight Highly Cited Articles Published in This Section ofBrain sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Sleep deprivation often leads to marked neurobehavioral and cognitive deficits, yet few well-defined interventions exist to address these effects. Dexmedetomidine (DEX), a highly selective α Methods: In this study, a rapid eye movement sleep deprivation (RSD) rat model was created using a modified multi-platform method. The influence of dexmedetomidine (DEX) on hippocampal tissue morphology, the BDNF/TrkB signaling pathway, and cognitive function was then evaluated. Group comparisons were analyzed using one-way ANOVA followed by appropriate post hoc tests. Results: In comparison with the control group, DEX significantly alleviated the impaired spatial learning and memory as reflected escape latency and increased the time spent in the garget quadrant. ANA-12 reversed these improvements, indicating DEX's cognitive benefits. HE staining showed that DEX protected neurons from RSD-induced injury by preserving structural integrity and TUNEL assay demonstrated reduced neuron apoptosis in the DEX group. Co-treatment with ANA-12 abolished these protective effects, resulting in neuronal damage and apoptosis levels similar to those observed in RSD rats. Moreover, compared with the level of TNA alpha in RSD rats, IL 6, IL 1beta and MDA levels were lower in the hippocampus of DEX group, while SOD activity was enhanced. Western blot analysis revealed that DEX increased hippocampal BDNF (0.586 ± 0.036 vs 0.315 ± 0.034, ~1.86‑fold, P < 0.01), TrkB (0.774 ± 0.039 vs 0.518 ± 0.033, ~1.49‑fold, P < 0.01) and pro-TrkB expression. However, co-administration of ANA‑12 abolished these effects, returning expression levels close to those in the RSD group, implying that DEX's neuroprotection is mediated via the BDNF/TrkB pathway. Conclusion: These findings indicate that DEX exerts neuroprotective effects in RSD by activating the BDNF/TrkB pathway, offering valuable evidence for DEX-based therapeutic approaches to sleep deprivation-related brain injury.
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.