ArticleFrontiers in behavioral neuroscience2026
Median nerve electrical stimulation promotes myelin regeneration through regulating miR-1-3p/BDNF/TrkB-MAPK pathway in a transient cerebral ischemia rat model.
Article in Frontiers in behavioral neuroscience, 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
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Median nerve electrical stimulation (MNES) has emerged as a promising peripheral neuromodulatory strategy for improving motor recovery after ischemic stroke. Because the median nerve provides strong afferent input to central sensorimotor pathways, MNES may influence post-stroke neural repair beyond symptomatic motor modulation. However, the molecular mechanisms linking MNES to myelin repair remain unclear. Brain-derived neurotrophic factor (BDNF) is closely involved in neuronal survival, plasticity, and myelin remodeling, and bioinformatic analysis identified BDNF as a putative target of miR-1-3p. Therefore, this study investigated whether MNES-associated neurological recovery and myelin repair after ischemic stroke involve modulation of the miR-1-3p/BDNF/TrkB-MAPK pathway. Methods: Adult male Sprague-Dawley rats were subjected to middle cerebral artery occlusion/reperfusion (MCAO/R), followed by MNES every other day for seven sessions. Neurological function, infarct injury, neuronal survival, neuroinflammation, myelin integrity, and pathway-related molecular changes were evaluated using behavioral, histological, ultrastructural, RT-qPCR, and Western blot analyses. Results: MNES was associated with improved neurological performance, reduced infarct injury, better preservation of myelin structure, decreased miR-1-3p expression, and increased BDNF, TrkB, and MAPK expression. In miR-1-3p modulation experiments, miR-1-3p antagomir partially mimicked the neuroprotective and myelin-related effects observed after MNES, whereas miR-1-3p agomir attenuated several MNES-associated benefits and reduced BDNF/TrkB-MAPK pathway-related protein expression. Conclusion: These findings suggest that MNES may support early neurological recovery and myelin repair after ischemic stroke, at least in part through involvement of the miR-1-3p/BDNF/TrkB-MAPK pathway. Further studies are required to confirm direct molecular targeting, long-term efficacy, safety, and translational relevance.
Indexed as
Identifiers
What Socratic 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 Socratic graph.