ArticleFrontiers in neurology
S-ketamine mitigates paclitaxel-induced pain-related anxiety-like behavior through downregulation of mGluR5 and activation of the BDNF/TrkB signaling pathway.
Article in Frontiers in neurology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Esketamine Alleviates Neuropathic Pain and Inflammation via miR-153-3p/AKT3 in CCI Rats.Pain research & management · 2026Article
- Everolimus Attenuates Salicylate-Induced Tinnitus-Like Behavior and Auditory Cortical Hyperexcitability.Drug design, development and therapy · 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
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Paclitaxel (PTX), a broad-spectrum anti-tumor drug, is extensively employed as a first-line chemotherapy for solid tumors, including lung and breast cancers. However, it induces chemotherapy-related pain and anxiety in over 53% of patients. S-ketamine, the S-enantiomer of ketamine, exerts rapid antidepressant effects. In this study, we established a PTX model to examine the effects of S-ketamine on pyramidal neurons in the prelimbic cortex (PrL) and the brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB) pathway, specifically investigating the role of metabotropic glutamate receptor 5 (mGluR5). Methods: A PTX-induced peripheral neuropathy and pain-related anxiety mouse model was established by intraperitoneal injection of PTX. Mechanical allodynia was assessed using the electronic von Frey test. Anxiety-like behaviors were evaluated using the elevated plus maze (EPM) and open field test (OFT) after S-ketamine treatment. After behavioral testing, electrophysiological recordings, immunofluorescence staining, and Western blotting analyses were performed, specifically targeting the PrL subregion of the medial prefrontal cortex (mPFC). Results: Compared with PTX-treated mice, S-ketamine administration resulted in significant improvements across behavioral, molecular, and electrophysiological dimensions: significantly increased mechanical withdrawal thresholds indicated alleviated neuropathic pain; Increased central area distance/total distance ratio in the OFT and prolonged open arm time in the EPM demonstrated reduced anxiety-like behaviors; concomitant decreases in mGluR5 expression and pyramidal neuron firing rates were observed alongside enhanced theta-gamma phase-amplitude coupling, and upregulation of BDNF and TrkB expression in the PrL was detected. Conclusion: S-ketamine mitigates PTX-induced mechanical allodynia and anxiety-like behaviors, an effect that is closely associated with the downregulation of mGluR5 and the concurrent modulation of the BDNF/TrkB signaling pathway in the PrL of the mPFC.
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.